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1. Part I
4/14/2010 2:36:28 AM
 
 
[Words list]

Konrad Lorenz, Adaptationism,  Adaptation,  Adaptedness and fitness,  Ideas of Adaptation, Changes in habitat,Habitat tracking, Genetic change, Red Queen hypothesis, co-adaptations, Mimicry, Internal adaptations, Compromise and conflict between adaptations, Pre-adaptation, Exaptation, Macroevolution, Speciation, Punctuated equilibrium, allopatric speciation, peripatric speciation, parapatric speciation, sympatric speciation, Speciation via polyploidization, Reinforcement (Wallace effect), Artificial speciation, Hybrid speciation, Gene transposition, Interspersed repeats, Human speciation, Natural selection, Genetic drift, Drift and fixation, heritable adaptations, Population bottleneck, Founder effect, Sewall-Wright effect, Canalisation, Phenotypic plasticity, Modularity, gene flow or gene migration, Barrier to gene flow, Gene flow in humans, Gene flow between species, Genetic pollution, Gene flow mitigation, Mutations, Neutral mutations, Weismann's "programmed death" theory, Mutation accumulation, Antagonistic pleiotropy, Disposable soma theory, altruistic suicide, group selection theories and Evolvability theories
 
 
 
 
 
Konrad Lorenz
 
Konrad Zacharias Lorenz (November 7, 1903 in Vienna 每 February 27, 1989 in Vienna) was an Austrian zoologist, animal psychologist, ornithologist, and Nobel Prize winner. He is often regarded as one of the founders of modern ethology, developing an approach that began with an earlier generation, including his teacher Oskar Heinroth. Lorenz studied instinctive behavior in animals, especially in greylag geese and jackdaws. Working with geese, he rediscovered the principle of imprinting in the behavior of nidifugous birds.
 
He wrote numerous books, some of which, such as King Solomon's Ring and On Aggression became popular reading. In later life his interest shifted to the study of man in society. At the request of his father, Adolf, Lorenz began a premedical curriculum in 1922 at Columbia University, but he returned to Vienna in 1923 to continue his studies at the University of Vienna. He graduated as Doctor of Medicine (MD) in 1928 and became an assistant professor at the Institute of Anatomy until 1935.He finished his zoological studies in 1933 and received his second doctorate (PhD).
 
In 1936, at an international scientific symposium on instinct, Lorenz met his great friend and colleague Niko Tinbergen. Together they studied geese - wild, domestic, and hybrid. One result of these studies was that Lorenz "realized that an overpowering increase in the drives of feeding as well as of copulation and a waning of more differentiated social instincts is characteristic of very many domestic animals." Lorenz began to suspect and fear "that analogous processes of deterioration may be at work with civilized humanity."
 
In 1940 he became a professor of psychology at the University of Königsberg. He was drafted into the Wehrmacht in 1941. He sought to be a motorcycle mechanic, but instead he was assigned as a medic. He was a prisoner of war in the Soviet Union from 1942 to 1948. In captivity he continued to work as a medical doctor and "got quite friendly with some Russians, mostly doctors." When he was repatriated, he was allowed to keep the manuscript of a book he had been writing, and his pet starling. He arrived back in Altenberg "with manuscript and bird intact." The manuscript became his book Behind the Mirror. The Max Planck Society established the Lorenz Institute for Behavioral Physiology in Buldern, Germany, in 1950.
 
In 1958, Lorenz transferred to the Max Planck Institute for Behavioral Physiology in Seewiesen. He shared the 1973 Nobel Prize in Physiology or Medicine "for discoveries in individual and social behavior patterns" with two other important early ethologists, Niko Tinbergen and Karl von Frisch. In 1969, he became the first recipient of the Prix mondial Cino Del Duca.Lorenz retired from the Max Planck Institute in 1973 but continued to research and publish from Altenberg (his family home, near Vienna) and Gr邦nau im Almtal in Austria.
 
Konrad Lorenz died on February 27, 1989, in Altenberg.
 
 
 
Adaptationism
Adaptationism is a set of methods in the evolutionary sciences for distinguishing the products of adaptation from traits that arise through other processes. It is employed in fields such as ethology and evolutionary psychology that are concerned with identifying adaptations. George Williams' Adaptation and Natural Selection was highly influential in its development, defining some of the heuristics, such as complex functional design, used to identify adaptations.
 
Adaptationism is sometimes characterized by critics as an unsubstantiated assumption that all or most traits are optimal adaptations. Critics (most notably Richard Lewontin and Stephen Jay Gould) contend that the adaptationists (John Maynard Smith, W.D. Hamilton and Richard Dawkins being frequent examples) have over-emphasized the power of natural selection to shape individual traits to an evolutionary optimum, and ignored the role of developmental constraints, and other factors to explain extant morphological and behavioural traits.
 
Adaptationists are accused by their critics of using ad-hoc "just-so stories" to make their theories unfalsifiable. The critics, in turn, have often been accused of attacking straw men, rather than the actual views of supposed adaptationists.
 
Adaptationist researchers respond by asserting that they, too, follow George Williams' depiction of adaptation as an "onerous concept" that should only be applied in light of strong evidence. This evidence can be generally characterized as the successful prediction of novel phenomena based on the hypothesis that design details of adaptations should fit a complex evolved design to respond to a specific set of selection pressures. In evolutionary psychology, researchers such as David Buss contend that the bulk of research findings that were uniquely predicted through adaptationist hypothesizing comprise evidence of the methods' validity.
 
The debate has occasionally been colored by a political subtext, with the Marxist-influenced Lewontin and Gould accusing sociobiologists of employing adaptationist fallacies in supporting socially regressive views of biological determinism. The history of this debate, and others related to it, are covered in detail by Cronin (1992) and Segerstråle (2000). Adaptationists such as Steven Pinker have also suggested that the debate has a strong ad hominem component. Some suggest that the controversy over the relative importance of various factors would be a quiet debate over subtleties if the critics were less prone to caricaturing their opponents.
 

 
Adaptation
Adaptation is one of the basic phenomena of biology. It is the process whereby an organism becomes better suited to its habitat. Also, the term adaptation may refer to a characteristic which is especially important for an organism's survival. For example, the adaptation of horses' teeth to the grinding of grass, or their ability to run fast and escape predators. Such adaptations are produced in a variable population by the better suited forms reproducing more successfully, that is, by natural selection.
The significance of an adaptation can only be understood in relation to the total biology of the species. Julian Huxley
Adaptation is, first of all, a process, rather than a physical part of a body. The distinction may be seen in an internal parasite (such as a fluke), where the bodily structure is greatly simplified, but nevertheless the organism is highly adapted to its unusual environment. From this we see that adaptation is not just a matter of visible traits: in such parasites critical adaptations take place in the life-cycle, which is often quite complex. However, as a practical term, adaptation is often used for the product: those features of a species which result from the process. Many aspects of an animal or plant can be correctly called adaptations, though there are always some features whose function is in doubt. By using the term adaptation for the evolutionary process, and adaptive trait for the bodily part or function (the product), the two senses of the word may be distinguished.
Adaptation may be seen as one aspect of a two-stage process. First, there is speciation (species-splitting or cladogenesis), caused by geographical isolation or some other mechanism. Second, there follows adaptation, driven by natural selection. Something like this must have happened with Darwin's finches, and there are many other examples. The present favourite is the evolution of cichlid fish in African lakes, where the question of reproductive isolation is much more complex.
Another great principle is that an organism must be viable at all stages of its development and at all stages of its evolution. This is obviously true, and it follows that there are constraints on the evolution of development, behaviour and structure of organisms. The main constraint, over which there has been much debate, is the requirement that changes in the system during evolution should be relatively small changes, because the body systems are so complex and interlinked. This is a sound principle, though there may be rare exceptions: polyploidy in plants is common, and the symbiosis of micro-organisms that formed the eukaryota is a more exotic example.
All adaptations help organisms survive in their ecological niches. These adaptative traits may be structural, behavioral or physiological. Structural adaptations are physical features of an organism (shape, body covering, defensive or offensive armament); and also the internal organization). Behavioural adaptations are composed of inherited behaviour chains and/or the ability to learn: behaviours may be inherited in detail (instincts), or a tendency for learning may be inherited. Examples: searching for food, mating, vocalizations. Physiological adaptations permit the organism to perform special functions (for instance, making venom, secreting slime, phototropism); but also more general functions such as growth and development, temperature regulation, ionic balance and other aspects of homeostasis. Adaptation, then, affects all aspects of the life of an organism.
The following definitions are mainly due to Theodosius Dobzhansky.
1. Adaptation is the evolutionary process whereby an organism becomes better able to live in its habitat or habitats.
2. Adaptedness is the state of being adapted: the degree to which an organism is able to live and reproduce in a given set of habitats.
3. An adaptive trait is an aspect of the developmental pattern of the organism which enables or enhances the probability of that organism surviving and reproducing.
 
 
 
Adaptedness and fitness
 
From the above definitions, it is clear that there is a relationship between adaptedness and fitness (a key population genetics concept). Fitness is an estimate and a predictor of the rate of natural selection. What natural selection does is change the relative frequencies of alternative phenotypes, insofar as they are heritable. Although the two are connected, the one does not imply the other: a phenotype with high adaptedness may not have high fitness. Dobzhansky mentioned the example of the Californian redwood, which is highly adapted, but a relic species in danger of extinction. Elliott Sober commented that adaptation was a retrospective concept since it implied something about the history of a trait, whereas fitness predicts a trait's future.
1. Fitness. The degree of demographic difference among phenotypes. Usually a relative measure: the average contribution to a breeding population by a phenotype or a class of phenotypes. This is also known as Darwinian fitness, relative fitness, selective coefficient, and other terms.
2. Adaptedness. Usually an absolute measure: the average absolute contribution to the breeding population by a carrier of a phenotype or a class of phenotypes. Also known as absolute fitness, and as the Malthusian parameter when applied to species as a whole.

 
 
Ideas of Adaptation
 
Adaptation is the heart and soul of evolution. Niles Eldredge
Adaptation as a fact of life has been accepted by all the great thinkers who have tackled the world of living organisms. It is their explanations of how adaptation arises that separates these thinkers. A few of the most significant ideas:
1. Empedocles did not believe that adaptation required a final cause (~ purpose), but "came about naturally, since such things survived". Aristotle, however, did believe in final causes.
2. In natural theology, adaptation was interpreted as the work of a deity, even as evidence for the existence of God. William Paley believed that organisms were perfectly adapted to the lives they lead, an argument that shadowed Leibnitz, who had argued that God had brought about the best of all possible worlds. Voltaire's Dr Pangloss is a parody of this optimistic idea, and Hume also argued against design. The Bridgewater Treatises are a product of natural theology, though some of the authors managed to present their work in a fairly neutral manner. The series was lampooned by Robert Knox, who held quasi-evolutionary views, as the Bilgewater Treatises. Darwin broke with the tradition by emphasising the flaws and limitations which occurred in the animal and plant worlds.
3. Lamarck. His is a proto-evolutionary theory of the inheritance of acquired traits, whose main purpose is to explain adaptations by natural means. He proposed a tendency for organisms to become more complex, moving up a ladder of progress, plus "the influence of circumstances", usually expressed as use and disuse. His evolutionary ideas, and those of Geoffroy, fail because they cannot be reconciled with heredity. This was known even before Mendel by medical men interested in human races (Wells, Lawrence), and especially by Weismann.
Many other students of natural history, such as Buffon, accepted adaptation, and some also accepted evolution, without voicing their opinions as to the mechanism. This illustrates the real merit of Darwin and Wallace, and secondary figures such as Bates, for pushing forward a mechanism whose significance had only been glimpsed previously. A century later, experimental field studies and breeding experiments by such as Ford and Dobzhansky produced evidence that natural selection was not only the 'engine' behind adaptation, but was a much stronger force than had previously been thought.
 
 
 
Changes in habitat
 
Before Darwin, adaptation was seen as a fixed relationship between an organism and its habitat. It was not appreciated that as the climate changed, so did the habitat; and as the habitat changed, so did the biota. Also, habitats are subject to changes in their biota: for example, invasions of species from other areas. The relative numbers of species in a given habitat are always changing. Change is the rule, though much depends on the speed and degree of the change.
When the habitat changes, three main things may happen to a resident population: habitat tracking, genetic change or extinction. In fact, all three things may occur in sequence. Of these three effects, only genetic change brings about adaptation.
 

 
Habitat tracking
 
When a habitat changes, the most common thing to happen is that the resident population moves to another locale which suits it; this is the typical response of flying insects or oceanic organisms, who have wide (though not unlimited) opportunity for movement. This common response is called habitat tracking. It is one explanation put forward for the periods of apparent stasis in the fossil record (the punctuated equilibrium thesis).

 
 
Genetic change
 
Genetic change is what occurs in a population when natural selection acts on the genetic variability of the population. By this means, the population adapts genetically to its circumstances. Genetic changes may result in visible structures, or may adjust physiological activity in a way that suits the changed habitat.

 
 
Red Queen hypothesis
 
It is now clear that habitats and biota do frequently change. Therefore, it follows that the process of adaptation is never finally complete. Over time, it may happen that the environment changes little, and the species comes to fit its surroundings better and better. On the other hand, it may happen that changes in the environment occur relatively rapidly, and then the species becomes less and less well adapted. Seen like this, adaptation is a genetic tracking process, which goes on all the time to some extent, but especially when the population cannot or does not move to another, less hostile area. Also, to a greater or lesser extent, the process affects every species in a particular ecosystem.
Van Valen thought that even in a stable environment, competing species had to constantly adapt to maintain their relative standing. This became known as the Red Queen hypothesis.
 

 
co-adaptations
 
In co-evolution, where the existence of one species is tightly bound up with the life of another species, new or 'improved' adaptations which occur in one species are often followed by the appearance and spread of corresponding features in the other species. There are many examples of this; the idea emphasises that the life and death of living things is intimately connected, not just with the physical environment, but with the life of other species. These relationships are intrinsically dynamic, and may continue on a trajectory for millions of years, as has the relationship between flowering plants and insects (pollination).

 
 
Mimicry
 
Henry Walter Bates' work on Amazonian butterflies led him to develop the first scientific account of mimicry, especially the kind of mimicry which bears his name: Batesian mimicry. This is the mimicry by a palatable species of an unpalatable or noxious species. A common example seen in temperate gardens is the hover-fly, many of which 每 though bearing no sting 每 mimic the warning colouration of hymenoptera (wasps and bees). Such mimicry does not need to be perfect to improve the survival of the palatable species.
Bates, Wallace and M邦ller believed that Batesian and M邦llerian mimicry provided evidence for the action of natural selection, a view which is now standard amongst biologists. All aspects of this situation can be, and have been, the subject of research. Field and experimental work on these ideas continues to this day; the topic connects strongly to speciation, genetics and development.
 
 
Internal adaptations
 
There are some important adaptations to do with the overall coordination of the systems in the body. Such adaptations may have significant consequences. Examples, in vertebrates, would be temperature regulation, or improvements in brain function, or an effective immune system. An example in plants would be the development of the reproductive system in flowering plants. Such adaptations may make the clade (monophyletic group) more viable in a wide range of habitats. The acquisition of such major adaptations has often served as the spark for adaptive radiation, and huge success for long periods of time for a whole group of animals or plants.


 
Compromise and conflict between adaptations
 
All adaptations have a downside: horse legs are great for running on grass, but they can't scratch their backs; mammals' hair helps temperature, but offers a niche for ectoparasites; the only flying penguins do is under water. Adaptations serving different functions may be mutually destructive. Compromise and make-shift occur widely, not perfection. Selection pressures pull in different directions, and the adaptation that results is some kind of compromise.
Since the phenotype as a whole is the target of selection, it is impossible to improve simultaneously all aspects of the phenotype to the same degree. Ernst Mayr
Consider the antlers of the Irish elk, (often supposed to be far too large; in deer antler size has an allometric relationship to body size). Obviously antlers serve positively for defence against predators, and to score victories in the annual rut. But they are costly in terms of resource. Their size during the last glacial period presumably depended on the relative gain and loss of reproductive capacity in the population of elks during that time. Another example: camouflage to avoid detection is destroyed when vivid colors are displayed at mating time. Here the risk to life is counterbalanced by the necessity for reproduction.
The peacock's ornamental train (grown anew in time for each mating season) is a famous adaptation. It must reduce his maneuverability and flight, and is hugely conspicuous; also, its growth costs food resources. Darwin's explanation of its advantage was in terms of sexual selection: "it depends on the advantage which certain individuals have over other individuals of the same sex and species, in exclusive relation to reproduction." The kind of sexual selection represented by the peacock is called 'mate choice', with an implication that the process selects the more fit over the less fit, and so has survival value. The recognition of sexual selection was for a long time in abeyance, but has been rehabilitated. In practice, the blue peafowl Pavo cristatus is a pretty successful species, with a big natural range in India, so the overall outcome of their mating system is quite viable.
The conflict between the size of the human foetal brain at birth, (which cannot be larger than about 400ccs, else it will not get through the mother's pelvis) and the size needed for an adult brain (about 1400ccs), means the brain of a newborn child is quite immature. The most vital things in human life (locomotion, speech) just have to wait while the brain grows and matures. That is the result of the birth compromise. Much of the problem comes from our upright bipedal stance, without which our pelvis could be shaped more suitably for birth. Neanderthals had a similar problem.

 
 
Pre-adaptation
 
This occurs when a species or population has characteristics which (by chance) are suited for conditions which have not yet arisen. For example, the polyploid rice-grass Spartina townsendii is better adapted than either of its parent species to their own habitat of saline marsh and mud-flats. White Leghorn fowl are markedly more resistant to vitamin B deficiency than other breeds. On a plentiful diet there is no difference, but on a restricted diet this preadaptation could be decisive.
Pre-adaptation may occur because a natural population carries a huge quantity of genetic variability. In diploid eukaryotes, this is a consequence of the system of sexual reproduction, where mutant alleles get partially shielded, for example, by the selective advantage of heterozygotes. Micro-organisms, with their huge populations, also carry a great deal of genetic variability.
The first experimental evidence of the pre-adaptive nature of genetic variants in micro-organisms was provided by Salvador Luria and Max Delbr邦ck who developed fluctuation analysis, a method to show the random fluctuation of pre-existing genetic changes that conferred resistance to phage in the bacterium Escherichia coli.


 
Exaptation
 
Exaptation: Co-option of existing traits.The classic example is the ear ossicles of mammals, which we know from palaeontological and embryological studies originated in the upper and lower jaws and the hyoid of their Synapsid ancestors, and further back still were part of the gill arches of early fish. We owe this esoteric knowledge to the comparative anatomists, who, a century ago, were at the cutting edge of evolutionary studies. The word exaptation was coined to cover these shifts in function, which are surprisingly common in evolutionary history. The origin of wings from feathers that were originally used for temperature regulation is a more recent discovery.
 

 
Macroevolution
 
Macroevolution is a scale of analysis of evolution in separated gene pools. Macroevolutionary studies focus on change that occurs at or above the level of species, in contrast with microevolution, which refers to smaller evolutionary changes (typically described as changes in allele frequencies) within a species or population.
The process of speciation may fall within the purview of either, depending on the forces thought to drive it. Paleontology, evolutionary developmental biology, comparative genomics and genomic phylostratigraphy contribute most of the evidence for the patterns and processes that can be classified as macroevolution. An example of macroevolution is the appearance of feathers during the evolution of birds from theropod dinosaurs.
Russian entomologist Yuri Filipchenko (or Philipchenko, depending on the transliteration) first coined the terms "macroevolution" and "microevolution" in 1927 in his German language work, "Variabilität und Variation". Since the inception of the two terms, their meanings have been revised several times and even fallen into disfavor amongst scientists who prefer to speak of biological evolution as one process.
Within the Modern Synthesis school of thought, macroevolution is thought of as the compounded effects of microevolution. Thus, the distinction between micro- and macroevolution is not a fundamental one 每 the only difference between them is of time and scale. However, it should be noted that time is not a necessary distinguishing factor 每 macroevolution can happen without gradual compounding of small changes; whole-genome duplication can result in macroevolution occurring over a single generation - especially in plants. One of the most significant applications of this is found in the evolution of the vertebrates, which was mediated by duplications of the hox gene complex.
The term "macroevolution" frequently arises within the context of the evolution/creation debate, usually used by creationists alleging a significant difference between the evolutionary changes observed in field and laboratory studies and the larger scale macroevolutionary changes that scientists believe to have taken thousands or millions of years to occur. They may accept that evolutionary change is possible within species ("microevolution"), but deny that one species can evolve into another ("macroevolution").
These arguments are rejected by mainstream science, which holds that there is ample evidence that macroevolution has occurred in the past. The consensus of the scientific community is that the alleged micro-macro division is an artificial construct made by creationists and does not accurately reflect the actual processes of evolution. Evolutionary theory (including macroevolutionary change) remains the dominant scientific paradigm for explaining the origins of Earth's biodiversity. Its occurrence, while controversial with the public at large, is not disputed within the scientific community.
While details of macroevolution are continuously studied by the scientific community, the overall theory behind macroevolution (i.e. common descent) has been overwhelmingly consistent with empirical data. Predictions of empirical data from the theory of common descent have been so consistent that biologists often refer to it as the "fact of evolution".
Nicholas Matzke and Paul R. Gross have accused creationists of using "strategically elastic" definitions of micro- and macroevolution when discussing the topic. The actual definition of macroevolution accepted by scientists is "any change at the species level or above" (phyla, group, etc.) and microevolution is "any change below the level of species." Matzke and Gross state that many creationist critics define macroevolution as something that cannot be attained, as these critics describe any observed evolutionary change as "just microevolution".
 
 
 
Speciation
 
Speciation is the evolutionary process by which new biological species arise. The biologist Orator F. Cook seems to have been the first to coin the term 'speciation' for the splitting of lineages or 'cladogenesis,' as opposed to 'anagenesis' or 'phyletic evolution' occurring within lineages. Whether speciation is achieved normally via genetic drift or natural selection is the subject of much ongoing discussion. There are four geographic modes of speciation in nature, based on the extent to which speciating populations are geographically isolated from one another: allopatric, peripatric, parapatric, and sympatric. Speciation may also be induced artificially, through animal husbandry or laboratory experiments.
All forms of natural speciation have taken place over the course of evolution, though it still remains a subject of debate as to the relative importance of each mechanism in driving biodiversity.
One example of natural speciation is the diversity of the three-spined stickleback, a marine fish which, after the last ice age, has undergone speciation into new freshwater colonies in isolated lakes and streams. Over an estimated 10,000 generations, the sticklebacks show structural differences that are greater than those seen between different genera of fish including variations in fins, changes in the number or size of their bony plates, variable jaw structure, and color differences.

 
Punctuated equilibrium
 
There is debate as to the rate at which speciation events occur over geologic time. While some evolutionary biologists claim that speciation events have remained relatively constant over time, some palaeontologists such as Niles Eldredge and Stephen Jay Gould have argued that species usually remain unchanged over long stretches of time, and that speciation occurs only over relatively brief intervals, a view known as punctuated equilibrium

 
 
allopatric speciation
 
During allopatric speciation, a population splits into two geographically isolated allopatric populations (for example, by habitat fragmentation due to geographical change such as mountain building or social change such as emigration). The isolated populations then undergo genotypic and/or phenotypic divergence as they (a) become subjected to dissimilar selective pressures or (b) they independently undergo genetic drift. When the populations come back into contact, they have evolved such that they are reproductively isolated and are no longer capable of exchanging genes


 
peripatric speciation
 
In peripatric speciation, new species are formed in isolated, small peripheral populations which are prevented from exchanging genes with the main population. It is related to the concept of a founder effect, since small populations often undergo bottlenecks. Genetic drift is often proposed to play a significant role in peripatric speciation.

 
 
parapatric speciation
 
In parapatric speciation, the zones of two diverging populations are separate but do overlap. There is only partial separation afforded by geography, so individuals of each species may come in contact or cross the barrier from time to time, but reduced fitness of the heterozygote leads to selection for behaviours or mechanisms which prevent breeding between the two species.
Ecologists refer to parapatric and peripatric speciation in terms of ecological niches. A niche must be available in order for a new species to be successful.
 

 
sympatric speciation
 
In sympatric speciation, species diverge while inhabiting the same place. Often cited examples of sympatric speciation are found in insects which become dependent on different host plants in the same area. However, the existence of sympatric speciation as a mechanism of speciation is still hotly contested. People have argued that the evidences of sympatric speciation are in fact examples of micro-allopatric, or heteropatric speciation. The most widely accepted example of sympatric speciation is that of the cichlids of Lake Nabugabo in East Africa, which is thought to be due to sexual selection. Sympatric speciation refers to the formation of two or more descendant species from a single ancestral species all occupying the same geographic location.
Until recently, there has been a dearth of hard evidence that supports this form of speciation, with a general feeling that interbreeding would soon eliminate any genetic differences that might appear. But there has been at least one recent study that suggests that sympatric speciation has occurred in Tennessee cave salamanders.
The three-spined sticklebacks, freshwater fishes, that have been studied by Dolph Schluter (who received his Ph.D. for his work on Darwin's finches with Peter Grant) and his current colleagues in British Columbia, provide an intriguing example that is best explained by sympatric speciation.


 
Speciation via polyploidization
 
Polyploidy is a mechanism often attributed to causing some speciation events in sympatry. Not all polyploids are reproductively isolated from their parental plants, so an increase in chromosome number may not result in the complete cessation of gene flow between the incipient polyploids and their parental diploids.
Polyploidy is observed in many species of both plants and animals. In fact, it has been proposed that all of the existing plants and most of the animals are polyploids or have undergone an event of polyploidization in their evolutionary history. However, reproduction is often by parthenogenesis since polyploid animals are often sterile. Rare instances of polyploid mammals are known, but most often result in prenatal death.
 
 
Reinforcement (Wallace effect)
 
Reinforcement is the process by which natural selection increases reproductive isolation. It may occur after two populations of the same species are separated and then come back into contact. If their reproductive isolation was complete, then they will have already developed into two separate incompatible species. If their reproductive isolation is incomplete, then further mating between the populations will produce hybrids, which may or may not be fertile. If the hybrids are infertile, or fertile but less fit than their ancestors, then there will be no further reproductive isolation and speciation has essentially occurred (e.g., as in horses and donkeys.) The reasoning behind this is that if the parents of the hybrid offspring each have naturally selected traits for their own certain environments, the hybrid offspring will bear traits from both, therefore would not fit either ecological niche as well as the parents did. The low fitness of the hybrids would cause selection to favor assortative mating, which would control hybridization. This is sometimes called the Wallace effect after the evolutionary biologist Alfred Russel Wallace who suggested in the late 19th century that it might be an important factor in speciation. If the hybrid offspring are more fit than their ancestors, then the populations will merge back into the same species within the area they are in contact.


 
Artificial speciation
 
New species have been created by domesticated animal husbandry, but the initial dates and methods of the initiation of such species are not clear. For example, domestic sheep were created by hybridisation, and no longer produce viable offspring with Ovis orientalis, one species from which they are descended. Domestic cattle, on the other hand, can be considered the same species as several varieties of wild ox, gaur, yak, etc., as they readily produce fertile offspring with them.
The best-documented creations of new species in the laboratory were performed in the late 1980s. William Rice and G.W. Salt bred fruit flies, Drosophila melanogaster, using a maze with three different choices of habitat such as light/dark and wet/dry. Each generation was placed into the maze, and the groups of flies which came out of two of the eight exits were set apart to breed with each other in their respective groups. After thirty-five generations, the two groups and their offspring were isolated reproductively because of their strong habitat preferences: they mated only within the areas they preferred, and so did not mate with flies that preferred the other areas. The history of such attempts is described in Rice and Hostert (1993).
Diane Dodd was also able to show how mating preferences can develop from reproductive isolation in Drosophila pseudoobscura fruit flies after only eight generations using different food types, starch and maltose.
 
 
 
Hybrid speciation
 
Hybridization between two different species sometimes leads to a distinct phenotype. This phenotype can also be fitter than the parental lineage and as such natural selection may then favor these individuals. Eventually, if reproductive isolation is achieved, it may lead to a separate species. However, reproductive isolation between hybrids and their parents is particularly difficult to achieve and thus hybrid speciation is considered an extremely rare event. The Mariana Mallard arose from hybrid speciation.
Hybridization without change in chromosome number is called homoploid hybrid speciation. It is considered very rare but has been shown in Heliconius butterflies  and sunflowers. Polyploid speciation, which involves changes in chromosome number, is a more common phenomenon, especially in plant species.


 
Gene transposition
 
Theodosius Dobzhansky, who studied fruit flies in the early days of genetic research in 1930s, speculated that parts of chromosomes that switch from one location to another might cause a species to split into two different species. He mapped out how it might be possible for sections of chromosomes to relocate themselves in a genome. Those mobile sections can cause sterility in inter-species hybrids, which can act as a speciation pressure. In theory, his idea was sound, but scientists long debated whether it actually happened in nature. Eventually a competing theory involving the gradual accumulation of mutations was shown to occur in nature so often that geneticists largely dismissed the moving gene hypothesis.
However, 2006 research shows that jumping of a gene from one chromosome to another can contribute to the birth of new species. This validates the reproductive isolation mechanism, a key component of speciation.


 
Interspersed repeats
 
Interspersed repetitive DNA sequences function as isolating mechanisms. These repeats protect newly evolving gene sequences from being overwritten by gene conversion, due to the creation of non-homologies between otherwise homologous DNA sequences. The non-homologies create barriers to gene conversion. This barrier allows nascent novel genes to evolve without being overwritten by the progenitors of these genes. This uncoupling allows the evolution of new genes, both within gene families and also allelic forms of a gene. The importance is that this allows the splitting of a gene pool without requiring physical isolation of the organisms harboring those gene sequences.

 
 
Human speciation
 
Humans have genetic similarities with chimpanzees and gorillas, suggesting common ancestors. Analysis of genetic drift and recombination using a Markov model suggests humans and chimpanzees speciated apart 4.1 million years ago.
 
 
 
Natural selection
 
Natural selection is the process where heritable traits that make it more likely for an organism to survive and successfully reproduce become more common over successive generations of a population. It is a key mechanism of evolution.
The natural genetic variation within a population of organisms means that some individuals will survive and reproduce more successfully than others in their current environment. For example, the peppered moth exists in both light and dark colors in the United Kingdom, but during the industrial revolution many of the trees on which the moths rested became blackened by soot, giving the dark-colored moths an advantage in hiding from predators. This gave dark-colored moths a better chance of surviving to produce dark-colored offspring, and in just a few generations the majority of the moths were dark. Factors which affect reproductive success are also important, an issue which Darwin developed in his ideas on sexual selection.
Natural selection acts on the phenotype, or the observable characteristics of an organism, but the genetic (heritable) basis of any phenotype which gives a reproductive advantage will increase in frequency over the following generations. Over time, this process can result in adaptations that specialize organisms for particular ecological niches and may eventually result in the emergence of new species. In other words, natural selection is an important process (though not the only process) by which evolution takes place within a population of organisms.
Natural selection is one of the cornerstones of modern biology. The term was introduced by Charles Darwin in his groundbreaking 1859 book On the Origin of Species, in which natural selection was described by analogy to artificial selection, a process by which animals with traits considered desirable by human breeders are systematically favored for reproduction. The concept of natural selection was originally developed in the absence of a valid theory of heredity; at the time of Darwin's writing, nothing was known of modern genetics. The union of traditional Darwinian evolution with subsequent discoveries in classical and molecular genetics is termed the modern evolutionary synthesis. Natural selection remains the primary explanation for adaptive evolution.
 

 
Genetic drift
 
Genetic drift or allelic drift is the change in the relative frequency with which a gene variant (allele) occurs in a population that results from the fact that alleles in offspring are a random sample of those in the parents, and because of the role of chance in determining whether a given individual survives and reproduces. A population's allele frequency is the fraction of the gene copies that share a particular form.
Genetic drift is one of several evolutionary processes which lead to changes in allele frequencies over time. It may cause gene variants to disappear completely, and thereby reduce genetic variability.
In contrast to natural selection, which makes gene variants more common or less common due to their causal effects on reproductive success, the changes due to genetic drift are not driven by environmental or adaptive pressures, and may be beneficial, neutral, or detrimental to reproductive success.
The effect of genetic drift is larger in small populations, and smaller in large populations. Vigorous debates wage among scientists over the relative importance of genetic drift compared with natural selection. Ronald Fisher held the view that genetic drift plays at the most a minor role in evolution, and this remained the dominant view for several decades. In 1968 Motoo Kimura rekindled the debate with his neutral theory of molecular evolution which claims that most of the changes in the genetic material are caused by genetic drift.

 
 
Drift and fixation
 
The Hardy-Weinberg principle states that within sufficiently large, randomly mating populations the allele frequencies will tend to remain constant from one generation to the next unless the equilibrium is disturbed by migration, genetic mutation, or selection. However, there is no residual influence on this probability from the frequency distribution of alleles in the grandparent, or any earlier, population--only that of the parent population. The predicted distribution of alleles among the offspring is a memory-less probability as described in the Markov property. This means that the mathematical probabilities associated to the distribution of alleles in any generation are only derived from the distribution of alleles in the generation immediately prior. Thus when random fluctuations result in a deviation of the allele frequency between the parent and offspring generations, that deviation establishes new expected values for the allele distributions in the next generation to follow. It is impossible for a population to gain new alleles from the random shuffling of alleles passed to the next generation, but this shuffling can cause an existing allele to disappear.
Because random sampling can remove but not replace an allele, and because random declines or increases in allele frequency will influence the expected allele distributions for the next following generation, a population will tend towards genetic uniformity over time. When an allele reaches a frequency of 1 (100%) it is said to be "fixed" in the population and when an allele reaches a frequency of 0 (0%) it is lost. Once an allele becomes fixed, genetic drift comes to a halt, and the allele frequency cannot change unless a new allele is introduced in the population via mutation or gene flow. Thus even while genetic drift is a random, directionless process, it acts to eliminate genetic variation over time.

 
 
heritable adaptations
 
Although both processes drive evolution, genetic drift operates randomly while natural selection functions non-randomly. This is because natural selection emblematizes the ecological interaction of a population, whereas drift is regarded as a sampling procedure across successive generations without regard to fitness pressures imposed by the environment. While natural selection is directioned, guiding evolution by impelling heritable adaptations to the environment, genetic drift has no direction and is guided only by the mathematics of chance.
As a result, drift acts upon the genotypic frequencies within a population without regard their relationship to the phenotype. Changes to the genotype caused by genetic drift may or may not result in changes to the phenotype. In drift each allele in a population is randomly and independently affected, yet the fluctuations in their allele frequencies are all driven in a quantitatively similar manner. Drift is blind with respect to any advantage or disadvantage the allele may bring. Alternatively, natural selection acts directly on the phenotype and indirectly on its underlying genotype. Selection responds specifically to the adaptive advantage or disadvantage presented by a phenotypic trait, and thus affects genes differentially. Selection indirectly rewards the alleles that develop adaptively advantageous phenotypes; with an increase in reproductive success for the phenotype comes an increase in allele frequency. By the same token, selection lowers the frequencies for alleles that cause unfavorable traits, and ignores those which are neutral.
In natural populations, genetic drift and natural selection do not act in isolation; both forces are always at play. However, the degree to which alleles are affected by drift or selection varies according to population size. The statistical effect of sampling error during the reproduction of alleles is much greater in small populations than in large ones. When populations are very small, drift will predominate, and may preserve unfavorable alleles and eliminate favorable ones. Weak selective effects may not be seen at all, as the small changes in frequency they would produce are overshadowed by drift.
In a large population, the probability of sampling error is small and little change to the allele frequencies is expected, even over many generations. Even weak selection forces acting upon an allele will push its frequency upwards or downwards (depending on whether the allele's influence is beneficial or harmful). However, in cases where the allele frequency is very small, drift can also overpower selection--even in large populations. For example, while disadvantageous mutations are usually eliminated quickly in large populations, new advantageous mutations are almost as vulnerable to loss through genetic drift as are neutral mutations. It is not until the allele frequency for the advantageous mutation reaches a certain threshold that genetic drift will have little effect.

 
 
Population bottleneck
 
In one particular type of genetic drift, a population bottleneck, a larger population contracts to a significantly smaller size over a short period of time due to some random environmental event. In a true population bottleneck, the odds for survival of any member of the population are purely random, and are not improved by any particular inherent genetic advantage. The bottleneck can result in a sudden and radical change in the allele frequency completely independent of selection. And its impact can be sustained, even when the bottleneck is caused by a one-time event such as a natural catastrophe. Even when the allele frequency of the original population is carried forward in the surviving population, a radical reduction in population size increases the likelihood of further allele fluctuation from drift in generations to come.
A population's genetic variation can be greatly reduced by a bottleneck, and even beneficial adaptations may be permanently eliminated. The loss of variation leaves the surviving population vulnerable to any new selection pressures such as disease, climate change or shift in the available food source, because adapting in response to environmental changes requires sufficient genetic variation in the population for natural selection to take place.
There have been many known cases of population bottleneck in the recent past. Prior to the arrival of Europeans, North American prairies were habitat for millions of greater prairie chickens. In Illinois alone, their numbers plummeted from about 100 million birds in 1900 to about 50 in the 1990s. The declines in population resulted from hunting and habitat destruction, but the random consequence has been a loss of most of the species' genetic diversity. DNA analysis comparing birds from the mid century to birds in the 1990s documents a steep decline the genetic variation in just in the latter few decades. Currently the greater prairie chicken is experiencing low reproductive success.
Over-hunting also caused a severe population bottleneck in the northern elephant seal in the 19th century. Their resulting decline in genetic variation can be deduced by comparing it to that of the southern elephant seal which were not so aggressively hunted.
 

 
Founder effect
 
The founder effect is a special case of genetic drift, occurring when a small group in a population splinters off from the original population and forms a new one. The random sample of alleles in the just formed new colony is expected to grossly misrepresent the original population in at least some respects. It is even possible that the number of alleles for some genes in the original population is larger than the number of gene copies in the founders, making complete representation impossible. When a newly formed colony is small, its founders can strongly affect the population's genetic make-up far into the future.
A well documented example is found in the Amish migration to Pennsylvania in 1744. Two members of the new colony shared the recessive allele for Ellis-van Creveld syndrome. Members of the colony and their descendants tend to be religious isolates and remain relatively insular. As a result of many generations of inbreeding, Ellis-van Creveld syndrome is now much more prevalent among the Amish than in the general population.
The difference in gene frequencies between the original population and colony may also trigger the two groups to diverge significantly over the course of many generations. As the difference, or genetic distance, increases, the two separated populations may become distinct, both genetically and phenetically, although not only genetic drift but also natural selection, gene flow and mutation will all contribute to this divergence. This potential for relatively rapid changes in the colony's gene frequency led most scientists to consider the founder effect (and by extension, genetic drift) a significant driving force in the evolution of new species. Sewall Wright was the first to attach this significance to random drift and small, newly isolated populations with his shifting balance theory of speciation. Following after Wright, Ernst Mayr created many persuasive models to show that the decline in genetic variation and small population size following the founder effect were critically important for new species to develop. However there is much less support for this view today since the hypothesis has been tested repeatedly through experimental research and the results have been equivocal at best.


 
Sewall-Wright effect
 
The concept for genetic drift was first introduced by one of the founders in the field of population genetics, Sewall Wright. His first use of the term "drift" was in 1929, though at the time he was using it in the sense of a directed process of change, or natural selection. Later that year he used it to refer to a purely random process, or change due to the effects of sampling error. It came to be known as the "Sewall-Wright effect", though he was never entirely comfortable to see his name given to it. He preferred "drifting at random", and "drift" came to be adopted as a technical term in the stochastic sense exclusively.
In the early days of the modern evolutionary synthesis, scientists were just beginning to blend the new science of population genetics with Charles Darwin's theory of natural selection. Working within this new framework, Wright focused on the effects of inbreeding on small relatively isolated populations. He introduced the concept of an adaptive landscape in which phenomena such as cross breeding and genetic drift in small populations could push them away from adaptive peaks, which would in turn allow natural selection to push them towards new adaptive peaks. Wright thought smaller populations were more suited for natural selection because "inbreeding was sufficiently intense to create new interaction systems through random drift but not intense enough to cause random nonadaptive fixation of genes."
Wright's views on the role of genetic drift in the evolutionary scheme were controversial almost from the very beginning. One of the most vociferous and influential critics was colleague Ronald Fisher. Fisher conceded genetic drift played some role in evolution, but an insignificant one. Fisher has been accused of misunderstanding Wright's views because in his criticisms Fisher seemed to argue Wright had rejected selection almost entirely. To Fisher, viewing the process of evolution as a long, steady, adaptive progression was the only way to explain the ever increasing complexity from simpler forms. But the debates have continued between the "gradualists" and those who lean more toward the Wright model of evolution where selection and drift together play an important role. Richard Dawkins is one scientist aligned more with Fisher. Dawkins considers drift important in small or isolated populations, but much less so than natural selection. The work of Ernst Mayr, a proponent of idea that the founder effect could give rise to new lineages of species, lends support to the Wright model.
 
 
 
Canalisation
 
Canalisation  is a measure of the ability of a population to produce the same phenotype regardless of variability of its environment or genotype. The term canalisation was coined by C. H. Waddington, who also helped explain its developmental mechanisms. He also introduced the epigenetic landscape, in which a canalised trait is illustrated as a valley enclosed by high ridges, safely guiding the phenotype to its "fate".
Canalisation is divided into genetic and environmental canalisation; genetic canalisation refers to distinct genotypes producing the same phenotype, while environmental canalisation refers to the same genotype producing the same phenotype in spite of environmental variation.
A recent molecular example was given by Rutherford & Lindquist. Hsp90 is a chaperone protein, monitoring the correct folding of some polypeptides into proteins. Rutherford & Lindquist heat shocked drosophila embryos, therefore presumably recruiting a portion of cytoplasmic Hsp90 to respond to the stress. The decrease in the normal monitoring activity of Hsp90 resulted in many morphological changes in the adult flies. These changes would disappear at the next generation in the absence of the stress. A genetic reduction in HSP90 function had similar effects. One possible conclusion is that Hsp90 is buffering mutations: flies have accumulated many mutations, but their effect is masked by Hsp90. To test this hypothesis, they crossed flies displaying morphological changes, mimicking natural selection during big environmental changes. The resulting flies displayed morphological changes even in the absence of heat shock or mutant alleles : the amount of accumulated mutations in these flies had overcome the buffering capacity of Hsp90 and these flies had changed their epigenetic valley. This, then, is an example of genetic canalisation.

 
 
Phenotypic plasticity
 
Phenotypic plasticity is the ability of an organism to change its phenotype in response to changes in the environment. Such plasticity in some cases expresses as several highly morphologically distinct results; in other cases, a continuous norm of reaction describes the functional interrelationship of a range of environments to a range of phenotypes. The term was originally conceived in the context of development, but is now more broadly applied to include changes that occur during the adult life of an organism, such as behaviour.
Organisms may differ in the degree of phenotypic plasticity they display when exposed to the same environmental change. Hence, phenotypic plasticity can evolve and be adaptive if fitness is increased by changing phenotype. In general, sustained directional selection is predicted to increase plasticity in that same direction.
Some responses will be similar in all organisms, for example in organisms that do not thermoregulate, as temperatures change lipids in the cell membrane must be altered by creating more double bonds (when temperatures decrease) or removing them (when temperatures increase).
Generally phenotypic plasticity is more important for immobile organisms (for example plants) than mobile organisms (animals). This is because immobile organisms have to adapt to their environment or they will die whereas mobile organisms are able to move to away from a damaging environment. Examples of phenotypic plasticity in plants include allocating more resources towards the roots in soils that contain low concentration of nutrients and changing leaf size and thickness. The transport proteins present in roots are also changed depending on the concentration of the nutrient and the salinity of the soil. Some plants, for example Mesembryanthemum crystallinum are able to alter their photosynthetic pathways to use less water when they become water or salt stressed.
In epidemiology, a theory is that rising incidences of coronary heart disease and type II diabetes in human populations undergoing industrialization is due to a mismatch between a metabolic phenotype determined in development and the nutritional environment an individual is subsequently exposed to. This is known as the 'thrifty phenotype' hypothesis.

 
 
Modularity
 
Many organisms consist of modules, both anatomically and in their metabolism. Anatomical modules are usually segments or organs. When we look at illustrations of metabolic reactions, we find that they, too, are modular: we can clearly identify, for instance, the citric acid cycle as a complex network that has only a few interfaces with other such modules. This principle holds true at various different scales: we can identify smaller modules within such larger networks that are similarly self-contained. We say that metabolic modularity is scale-free.
In addition to showing scalefree and small world properties, biological networks appear to exhibit modularity in topological structure. In the field of network biology, the definition of nodes and edges in a given network depends on the type of network examined. For example, in a protein interaction network, nodes correspond with individual proteins and edges represent the interactions between them (either through direct physical interaction, or compound-mediated). Metabolic networks, on the other hand, contain metabolite nodes and edges that represent the specific enzymes that connect them (in catalyzing biochemical reactions). As with any type of network, modularity in biological networks allows sub-groups of nodes and edges to function in a semi-autonomous fashion.
The concept of modularity resurfaces at the scale of organs and developmental units. Why are there distinct cell types organised into spatial aggregations (organs), and what are the benefits of having a segmented body plan, containing different modules (for instance, thoracic and abdominal segments in an arthropod) and where one of the possible differences between species is in the number of each type of module they possess?
Interestingly, this property has led researchers to suggest that modularity imparts a certain degree of evolvability to a system by allowing specific features (i.e. network sub-groups) to undergo changes without substantially altering the functionality of the entire system. Essentially, each module is free to evolve within, so long as the interfaces between modules remain consistent. This would suggest that the metabolic pathways at the edges between modules are relatively more constrained. It is thought that there exists an optimal degree of modularity for each given organism.

 
 
gene flow or gene migration
 
In population genetics, gene flow (also known as gene migration) is the transfer of alleles of genes from one population to another.Migration into or out of a population may be responsible for a marked change in allele frequencies (the proportion of members carrying a particular variant of a gene). Immigration may also result in the addition of new genetic variants to the established gene pool of a particular species or population.
There are a number of factors that affect the rate of gene flow between different populations. One of the most significant factors is mobility, as greater mobility of an individual tends to give it greater migratory potential. Animals tend to be more mobile than plants, although pollen and seeds may be carried great distances by animals or wind.
Maintained gene flow between two populations can also lead to a combination of the two gene pools, reducing the genetic variation between the two groups. It is for this reason that gene flow strongly acts against speciation, by recombining the gene pools of the groups, and thus, repairing the developing differences in genetic variation that would have led to full speciation and creation of daughter species.Example: If a field of genetically modified corn is grown alongside a field of non-genetically modified corn, pollen from the former is likely to fertilize the latter.

 
 
Barrier to gene flow
 
Physical barriers to gene flow are usually, but not always, natural. They may include impassable mountain ranges, oceans, or vast deserts. In some cases, they can be artificial, man-made barriers, such as the Great Wall of China, which has hindered the gene flow of native plant populations. Samples of the same species which grow on either side have been shown to have developed genetic differences, because there is no gene flow to provide recombination of the gene pools.
Barriers to gene flow need not always to be physical. Species can live in the same environment, yet show very limited gene flow due to limited hybridization or hybridization yielding unfit hybrids.


 
Gene flow in humans
Gene flow has been observed in humans. For example, in the United States, gene flow was observed between a white European population and a black West African population, which were recently brought together. In West Africa, where malaria is prevalent, the Duffy antigen provides some resistance to the disease, and this allele is thus present in nearly all of the West African population. In contrast, Europeans have either the allele Fya or Fyb, because malaria is almost non-existent. By measuring the frequencies of the West African and European groups, scientists found that the allele frequencies became mixed in each population because of movement of individuals. It was also found that this gene flow between European and West African groups is much greater in the Northern U.S. than in the South.

 
Gene flow between species
 
Gene flow can occur between species, either through hybridization or gene transfer from bacteria or virus to new hosts.
Gene transfer, defined as the movement of genetic material across species boundaries, which includes horizontal gene transfer, antigenic shift, and reassortment is sometimes an important source of genetic variation. Viruses can transfer genes between species. Bacteria can incorporate genes from other dead bacteria, exchange genes with living bacteria, and can exchange plasmids across species boundaries. "Sequence comparisons suggest recent horizontal transfer of many genes among diverse species including across the boundaries of phylogenetic "domains". Thus determining the phylogenetic history of a species can not be done conclusively by determining evolutionary trees for single genes."
Biologist Gogarten suggests "the original metaphor of a tree no longer fits the data from recent genome research". Biologists [should] instead use the metaphor of a mosaic to describe the different histories combined in individual genomes and use the metaphor of an intertwined net to visualize the rich exchange and cooperative effects of horizontal gene transfer.
"Using single genes as phylogenetic markers, it is difficult to trace organismal phylogeny in the presence of HGT [horizontal gene transfer]. Combining the simple coalescence model of cladogenesis with rare HGT [horizontal gene transfer] events suggest there was no single last common ancestor that contained all of the genes ancestral to those shared among the three domains of life. Each contemporary molecule has its own history and traces back to an individual molecule cenancestor. However, these molecular ancestors were likely to be present in different organisms at different times."

 
 
Genetic pollution
 
Purebred, naturally-evolved, region-specific, wild species can be threatened with extinction in a big way through the process of genetic pollution, i.e., uncontrolled hybridization, introgression and genetic swamping which leads to homogenization or replacement of local genotypes as a result of either a numerical and/or fitness advantage of introduced plant or animal. Nonnative species can bring about a form of extinction of native plants and animals by hybridization and introgression either through purposeful introduction by humans or through habitat modification, bringing previously isolated species into contact. These phenomena can be especially detrimental for rare species coming into contact with more abundant ones where the abundant ones can interbreed with them swamping the entire rarer gene pool creating hybrids thus driving the entire original purebred native stock to complete extinction. Attention has to be focused on the extent of this under appreciated problem that is not always apparent from morphological (outward appearance) observations alone. Some degree of gene flow may be a normal, evolutionarily constructive process, and all constellations of genes and genotypes cannot be preserved however, hybridization with or without introgression may, nevertheless, threaten a rare species' existence.

 
Gene flow mitigation
 
When cultivating genetically modified (GM) plants or livestock, it becomes necessary to prevent "genetic pollution" i.e. their genetic modification from reaching other conventionally hybridized or wild native plant and animal populations by using gene flow mitigation usually through unintentional cross pollination and crossbreeding. Reasons to limit gene flow may include biosafety or agricultural co-existence, in which GM and non-GM cropping systems work side by side.
Scientists in several large research programmes are investigating methods of limiting gene flow in plants. Among these programmes are Transcontainer, which investigates methods for biocontainment, SIGMEA, which focuses on the biosafety of genetically modified plants, and Co-Extra, which studies the co-existence of GM and non-GM product chains.
Generally, there are three approaches to gene flow mitigation: keeping the genetic modification out of the pollen, preventing the formation of pollen, and keeping the pollen inside the flower.
The first approach requires transplastomic plants. In transplastomic plants, the modified DNA is not situated in the cell's nucleus but is present in plastids, which are cellular compartments outside the nucleus. An example for plastids are chloroplasts, in which photosynthesis occurs. In some plants, the pollen does not contain plastids and, consequently, any modification located in plastids cannot be transmitted by the pollen.
The second approach relies on male sterile plants. Male sterile plants are unable to produce functioning flowers and therefore cannot release viable pollen. Cytoplasmic male sterile plants are known to produce higher yields. Therefore, researchers are trying to introduce this trait to genetically modified crops.
The third approach works by preventing the flowers from opening. This trait is called cleistogamy and occurs naturally in some plants. Cleistogamous plants produce flowers which either open only partly or not at all. However, it remains unclear how reliable cleistogamy is for gene flow mitigation: a Co-Extra research project on rapeseed investigating the matter has published preliminary results which cast doubt on the attainment of a high degree of reliability.
 

 
Mutations
 
In biology, mutations are changes to the nucleotide sequence of the genetic material of an organism. Mutations can be caused by copying errors in the genetic material during cell division, by exposure to ultraviolet or ionizing radiation, chemical mutagens, or viruses, or can be induced by the organism itself, by cellular processes such as hypermutation. In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germ line mutations, which can be passed on to descendants through the reproductive cells, and somatic mutations, which involve cells outside the dedicated reproductive group and which are not usually transmitted to descendants. If the organism can reproduce asexually through mechanisms such as cuttings or budding the distinction can become blurred. For example, plants can sometimes transmit somatic mutations to their descendants asexually or sexually where flower buds develop in somatically mutated parts of plants. A new mutation that was not inherited from either parent is called a de novo mutation. The source of the mutation is unrelated to the consequence, although the consequences are related to which cells were mutated.
Mutations create variation within the gene pool. Less favorable (or deleterious) mutations can be reduced in frequency in the gene pool by natural selection, while more favorable (beneficial or advantageous) mutations may accumulate and result in adaptive evolutionary changes. For example, a butterfly may produce offspring with new mutations. The majority of these mutations will have no effect; but one might change the color of one of the butterfly's offspring, making it harder (or easier) for predators to see. If this color change is advantageous, the chance of this butterfly surviving and producing its own offspring are a little better, and over time the number of butterflies with this mutation may form a larger percentage of the population.
Mutation is generally accepted by the scientific community as the mechanism upon which natural selection acts, providing the advantageous new traits that survive and multiply in offspring or disadvantageous traits that die out with weaker organisms.


 
Neutral mutations
 
Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no significant effect on an organism's fitness. Also, DNA repair mechanisms are able to mend most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.


 
Weismann's "programmed death" theory
 
Enquiry into the evolution of ageing aims to explain why almost all living things weaken and die with age. There is not yet agreement in the scientific community on a single answer. The evolutionary origin of senescence remains a fundamental unsolved problem in biology.
Historically, ageing was first likened to "wear and tear": living bodies get weaker just as with use a knife's edge becomes dulled or with exposure to air and moisture iron objects rust. But this idea was discredited in the 19th century when the second law of thermodynamics was formalized. Entropy (disorder) must increase inevitably within a closed system, but living beings are not closed systems. It is a defining feature of life that it takes in free energy from the environment and unloads its entropy as waste. Living systems can even build themselves up from seed, and routinely repair themselves. There is no thermodynamic necessity for senescence. In addition, generic damage or "wear and tear" theories could not explain why biologically similar organisms (e.g. mammals) exhibited such dramatically different life spans.
August Weismann was responsible for interpreting and formalizing the mechanisms of Darwinian evolution in a modern theoretical framework. In 1889, he theorized that ageing was part of life's program because the old need to remove themselves from the theater to make room for the next generation, sustaining the turnover that is necessary for evolution. This theory again has much intuitive appeal, but it suffers from having a teleological or goal-driven explanation. In other words, a purpose for ageing has been identified, but not a mechanism by which that purpose could be achieved. Ageing may have this advantage for the long-term health of the community; but that doesn't explain how individuals would acquire the genes that make them get old and die, or why individuals that had ageing genes would be more successful than other individuals lacking such genes. (In fact, there is every reason to think that the opposite is true: ageing decreases individual fitness.) Weismann disavowed his own theory before his life was over.
Theories suggesting that deterioration and death due to ageing are a purposeful result of an organism's evolved design (such as Weismann's "programmed death" theory) are referred to as theories of programmed ageing or adaptive ageing. The idea that the ageing characteristic was selected (an adaptation) because of its deleterious effect was largely discounted for much of the 20th century but is now experiencing a resurgence because of new empirical evidence as well as new thinking regarding the process of evolution.

 
Mutation accumulation
 
The first modern, successful theory of ageing was formulated by Peter Medawar in 1952. His idea was that ageing was a matter of neglect. Nature is a highly competitive place, and almost all animals in nature die before they attain old age. Therefore, there is not much motivation to keep the body fit for the long haul - not much selection pressure for traits that would maintain viability past the time when most animals would be dead anyway, killed by predators or disease or by accident.
Medawar's theory is referred to as Mutation Accumulation. The mechanism of action involves random, detrimental mutations of a kind that happen to show their effect only late in life. Unlike most detrimental mutations, these would not be efficiently weeded out by natural selection. Hence they would 'accumulate' and, perhaps, cause all the decline and damage that we associate with ageing.
This theory was further developed by George C. Williams in 1957, who noted that senescence may be causing many deaths, even if animals are not 'dying of old age'. In the earliest stages of senescence, an animal may lose a bit of its speed, and then predators will seize it first, while younger animals flee successfully. Or its immune system may decline, and it becomes the first to die of a new infection. Nature is such a competitive place, said Williams (turning Medawar's argument back at him), that even a little bit of senescence can be fatal; hence natural selection does indeed care; ageing isn't cost-free.
Williams's objection has turned out to be valid: Modern studies of demography in natural environments demonstrate that senescence does indeed make a substantial contribution to the death rate in nature. These observations cast doubt on Medawar's theory. Another problem with this theory became apparent in the late 1990s, when genomic analysis became widely available. It turns out that the genes that cause ageing are not random mutations; rather, these genes form tight-knit families that have been around as long as eukaryotic life. Baker's yeast, worms, fruit flies, and mice all share some of the same ageing genes.
Medawar's concept suggested that the evolution process was affected by the age at which an organism was capable of reproducing. Characteristics that adversely affected an organism prior to that age would severely limit the organism's ability to propagate its characteristics and thus would be highly "selected against" by natural selection. Characteristics that caused the same adverse effects that only appeared well after that age would have relatively little effect on the organism's ability to propagate. This concept fit well with the observed multiplicity of mammal life spans (and differing ages of sexual maturity) and is important to all of the subsequent theories of aging discussed below.


 
Antagonistic pleiotropy
 
Williams (1957) proposed his own theory, called antagonistic pleiotropy. Pleiotropy means one gene that has two or more effects on the phenotype. In antagonistic pleiotropy, one of these effects is beneficial and another is detrimental. In essence this refers to genes that offer benefits early in life, but exact a cost later on. If evolution is a race to have the most offspring the fastest, then enhanced early fertility could be selected even if it came with a price tag that included decline and death later on.
Antagonistic pleiotropy is the prevailing theory today, but this is largely by default, and not because the theory has been well verified. In fact, experimental biologists have looked for the genes that cause ageing, and since about 1990 the technology has been available to find them efficiently. Of the many ageing genes that have been reported, some seem to enhance fertility early in life, or to carry other benefits. But there are other ageing genes for which no such corresponding benefit has been identified. This is not what Williams predicted. This may be thought of as partial validation of the theory, but logically it cuts to the core premise: that genetic trade-offs are the root cause of ageing.
Another difficulty with antagonistic pleiotropy and other theories that suppose that ageing is an adverse side-effect of some beneficial function is that the linkage between adverse and beneficial effects would need to be rigid in the sense that the evolution process would not be able to eventually find a way to accomplish the benefit without incurring the adverse effect. Such a rigid relationship has not been experimentally demonstrated and, in general, evolution is obviously able to independently and individually adjust myriad organism characteristics.
In breeding experiments, Michael R. Rose selected fruit flies for long life span. Based on antagonistic pleiotropy, Rose expected that this would surely reduce their fertility. His team found that they were able to breed flies that lived more than twice as long as the flies they started with, but to their surprise, the long-lived, inbred flies actually laid more eggs than the short-lived flies. This was another setback for pleiotropy theory, though Rose maintains it may be an experimental artifact.


 
Disposable soma theory
 
A third mainstream theory of ageing, the Disposable soma theory, proposed in 1977 by Thomas Kirkwood, presumes that the body must budget the amount of energy available to it. The body uses food energy for metabolism, for reproduction, and for repair and maintenance. With a finite supply of food, the body must compromise, and do none of these things quite as well as it would like. It is the compromise in allocating energy to the repair function that causes the body gradually to deteriorate with age.
The term disposable soma came from the analogy with disposable products -- why spend money making something durable, if it will only be used for a limited amount of time?
The disposable soma theory has great appeal because its basis is so sensible and intuitive, but there are arguments against it. The theory clearly predicts that a shortage of food should make the compromise more severe all around; but in many experiments, ongoing since 1930, it has been demonstrated that animals live longer when fed substantially less than controls. This is the caloric restriction (CR) effect, and it cannot be easily reconciled with the Disposable Soma theory. Though by decreasing energy expenditure the damage generated (by free radicals for instance) is expected to be reduced and the total energy budget might indeed be reduced, but the investment in repair function might still be relatively the same. But dietary restriction has not been shown to increase lifetime reproductive success (fitness), because when food availability is lower reproductive output is also lower. So CR does thus not completely dismiss disposable theory.
Experimentally, some animals lose fertility when their life spans are extended by CR and some suffer no appreciable loss. Males, for example, typically remain fertile when underfed, while females do not. And, even females present an enigma because their fertility decline is not tightly coupled to their longevity gain. For example, in female mice that are restricted to 60% of a free-feeding diet, reproduction is shut down altogether. But female life span continues to increase linearly right up to the threshold of starvation - around 30% of free-feeding levels.
A difficulty with the disposable soma theory is that the energy required for maintenance and repair would appear to be relatively minor when compared to the energy required for gestation (repair should take less energy then producing an entire new organism). Yet gestating animals seem able to perform the maintenance while post-reproductive animals do not. A similar difficulty is that male animals seem to have similar life spans as females despite the apparently higher energy requirement for gestation and other reproductive activities.

 
 
altruistic suicide
 
A fundamental embarrassment for all three mainstream theories is that there appear to be 'deliberate' metabolic features, mechanisms that seem to have no other purpose than to cause death.
One is apoptosis, or programmed cell death. Apoptosis is responsible for killing infected cells, cancerous cells and cells that are simply in the wrong place during development. There are clear benefits to apoptosis, so the existence of apoptosis isn't a problem for evolutionary theory. The problem is that apoptosis seems to ramp up late in life and kill healthy cells, causing weakness and degeneration. And, paradoxically, apoptosis has been observed as a kind of 'altruistic suicide' in colonies of yeast under stress. This seems to be a direct hint that senescence arose because it conferred a direct evolutionary advantage, rather than some kind of side-effect of genes that have other evolutionary advantages (pleiotropy).
A second 'deliberate' mechanism is called replicative senescence or cellular senescence. Metaphorically, a cell may be said to 'count' (with its telomeres) the number of times that it has divided, and after a set number of replications, it languishes and dies. It has been proposed that this is a last-ditch protective mechanism against cancer. But this hypothesis fails because replicative senescence is far older than cancer. Many invertebrates experience replicative senescence, though they never die of cancer. Even one-celled organisms count replications, and will die if they don't replenish their telomeres with conjugation (sex).
More strictly, of course, cells cannot 'count' the number of times they have divided. Telomeres are not a counting mechanism, though they may be used to indicate the number of times a particular chromosome has been replicated. Cellular processes for genetic material replication occurs in both directions along DNA, 5' to 3' and on the other strand, 3' to 5'. As the 3' to 5' end is impossible for DNA polymerase to grab at the 1 base pair mark, a handful of basepairs (10-15) are cut off each replication. Over time, this cutting short of the DNA results in no telomeres, and the cell is unable to replicate that chromosome without cutting into genes.
The body's inflammation process exists to fight disease; but the system can turn against us, and does so increasingly with older age, causing heart disease and arthritis. This happens reliably enough that a low dose of aspirin each day (slightly toning down the inflammatory response in general) is sufficient to measurably reduce incidence of disease and death in older people. Is inflammation a function that goes haywire after a certain age? Or is self-destruction an adaptation?
The dilemma is that evolutionary theory says that what is maintained in a lineage is that which ensures the viability of an organism and its offspring. Ageing can only cut off an individual's capacity to reproduce. So, according to theory, ageing could only evolve as a side-effect, or epiphenomenon of selection. The disposable soma theory and antagonistic pleiotropy theory are examples in which a compensating individual benefit, compatible with classical evolution theory is proposed. Nevertheless, there is accumulated evidence that ageing looks like an adaptation in its own right, selected for its own sake.
Semelparous organisms and others that die suddenly following reproduction (e.g. salmon, octopus, marsupial mouse (Brown Antechinus), etc.) also represent instances of organisms whose design incorporates a life span limiting feature. Sudden death is more obviously an instance of programmed death or a purposeful adaptation than gradual aging. Biological elements clearly associated with evolved mechanisms such as hormone signalling have been identified in the death mechanisms of organisms such as the octopus.
For replicative senescence in one-celled organisms, telomeric ageing is clearly a 'feature' of the genetic software, not a bug. If ageing could evolve in one-celled organisms for the long-term good of the species, and despite its cost to the individual, then why not other forms of ageing that affect higher animals?

 
 
group selection theories and Evolvability theories
 
Evolved characteristics that limit life span in the absence of some individually beneficial compensating effect violate the generally understood classical rules of evolution. Believers in classical theory believe that any apparently evolved but individually adverse characteristic of an organism must have a compensating benefit to the ability of individual organisms to survive or reproduce. The disposable soma and antagonistic pleiotropy theories are examples of such thinking.
However, there were other apparently individually adverse organism observations such as altruism and sexual reproduction that also appeared to conflict with classical theory. In response to these other conflicts, adjustments to classical theory were proposed. Various group selection theories (beginning in 1962) propose that benefit to a group could offset the individually adverse nature of a characteristic such as altruism. The same principle could be applied to characteristics that limited life span and theories citing group benefits for limited life spans appeared.
Evolvability theories (beginning in 1995) suggest that a characteristic that increased an organism's ability to evolve could also offset an individual disadvantage and thus be evolved and retained. Multiple evolvability benefits of a limited life span were subsequently proposed in addition to those originally proposed by Weismann in 1882.
If organisms purposely limit their life spans via ageing or semelparous behavior, the associated evolved mechanisms could be very complex just as mechanisms that provide for mentation, vision, digestion, or other biological function are typically very complex. Such a mechanism could involve hormones, signalling, sensing of external conditions, and other complex functions typical of evolved mechanisms. Such complex mechanisms could explain all of the observations of ageing and semelparous behaviors.
Theories to the effect that ageing results by default (mutation accumulation) or is an adverse side-effect of some other function are logically much more limited and suffer when compared to empirical evidence of complex mechanisms. The choice of ageing theory therefore is logically essentially determined by one's position regarding evolutionary mechanisms.
In response to this dilemma, there are theorists who advocate a return to the ideas of Weismann: 'making room' for the next generation. Ageing helps keep the population diverse, mitigating the problem of inbreeding depression, the well-known tendency for offspring of closely-related parents to have excessive genetic defects. The problem with such theories is the same one that troubled Weismann: a good evolutionary theory should describe causes, not goals.



 
 
 

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