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Philosophy Discuss I Have Solved Evolution! in the Debate and Discussion forums; Still, you lack that one crucial fact... why evolution alters us correctly... how it does it.... how it manages to do it so quickly. going via the gene idea, then ...

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09-10-02

Still, you lack that one crucial fact... why evolution alters us correctly... how it does it.... how it manages to do it so quickly.

going via the gene idea, then that would mean as animals breed they gain better versions of themselves with each passing generation, and while that can loosely be proven nowadays, there is one problem, humans themselves have become odd, and we tend to mate with that which is akin to us. Smarts to smarts, strong to strong, beauty to beauty, thin to thin, etc.

In the past we would have just mated with whoever we saw, and, usually, whoever was strong enough to show off theirselves to the womenfolk. This means that we would have gained physical strength, but not mental strength, and yet we still did, and there is no explanation as to why.

In fact, the alteration which results in children being born so early was done mainly to stop children from popping out when they were too big to pop out, since our brain size had increased, yet nobody has any means by which to explain how this happened, since this would be a DRASTIC alteration in the woman's genes.


I guess that's a fine post.. ahh well.. *snores*


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09-10-02

It doesn't always alter for the better. SOmetimes it alters us in a potentially harmful way, either we will overcompensate for that potential harm or we will die from it, or it may never become an issue because of our static living conditions.



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09-11-02

Exactly what I mean guy person, that through out time, evolution has not always had "good" results per say.
Ok, if you think on is as if you were the planet. No seriously... if you were the planet trying to sustain all the various life forms, how would you control it? natural disasters, viral infections, bacterial growth... all the things that are generated by the planet. Now, here comes along a species, that has managed to evade many of your resources for population control, the only option that you have, is to create larger, better, stronger and more extreme options. Virus's have evolved, yes evolved, for a singular purpose besides the actual virus survival, to better perform the job it has. It's sole purpose can only be population control. Natural disasters seem to occur far more often than they did 20 years ago even. bacteria is more invasive to better fascilitate its role. Humans, threw the world a into a loop because of its evolution. It became stronger in general.
When you talk about strength being a primal factor, its true JP. However, hundreds of years ago, the mind and its attractions started to play the most significant role. Hence, our population in general is smaller in body size. In some countries, it got very small eons ago. If you look into history (what is available) you can see that the social and environmental conditions created changes in the populace. In egypt, before the introduction of other races into the gene pool... the people were very short IF you were part of the higher society. The lower class, were very large in conparison. We know this because we have many bodies to compare from different classes. Obviously,... the higher class didn't work as much physically... figures huh.

In Russia... the body size of its peoples was large, more physically massive for a longer period of time. It's children grew up faster, worked harder, and traveled longer distances.

Remember i'm talking about before mass country travel took effect. That rather mixes things up a bit.

Anyway, its to damned early in the morning for this If you look at history, and what physical data there is out there, you can see the changes to the human body and brain, in conjunction with the environment and society. It doesn't prove that the theory of evolution is 100% correct, but like I said before, it offers more plausible proof than any other theory out there. Just DNA isn't the only factor, it is the tool.


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09-11-02

You still haven't explained how it knew to evolve the human female body so that they would give birth long before they normally did.


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09-11-02

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How did it all happen so fast by mutations? You'd be talking about something wherein a series of accidents all happen in such a specific order and in an extremely short period of time, although it has been proven it takes a large period of time for mutational evolution such as you're talking about to occur.
No wrong. Mutation does not take a long time, but Evolution does. Evolution is the progression of a species of organisms, from one form to a superior form, which is better suited to survival in its environment, via mutation of genetic information, and inheritance of selected traits. If you read what I said you would realise that mutation does not always guarantee superiority, and more often than not mutations are detrimental, therefore the process of a single organism evolving may not take long(a single generation - take down syndrom people for instance, one single mistake[three instead of two of the 23rd chromosome] makes them so radically different from a normal person), but a whole population may take thousands even millions of years depending on reproduction rate and mating partner selection processes.



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09-11-02

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Still, you lack that one crucial fact... why evolution alters us correctly... how it does it.... how it manages to do it so quickly.
Because the advantageously mutated survive while the weak die.

Quote:
going via the gene idea, then that would mean as animals breed they gain better versions of themselves with each passing generation, and while that can loosely be proven nowadays, there is one problem, humans themselves have become odd, and we tend to mate with that which is akin to us. Smarts to smarts, strong to strong, beauty to beauty, thin to thin, etc.
Selection of mate criteria, animals in the wild possess selection criteria, usually the strongest in the attractive traits mate. Same is true for humans.
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In the past we would have just mated with whoever we saw, and, usually, whoever was strong enough to show off theirselves to the womenfolk. This means that we would have gained physical strength, but not mental strength, and yet we still did, and there is no explanation as to why.
Steadily the more intelligent human survived over the stupid, Neanderthal versus CroMagnon. The CroMagnon's wiped out the Neanderthal because they were smarter, and used tools, and used simple machines like the Wheel and the Incline Plane.
~~If you are a violently militant feminist you perhaps shouldn't read any further.~~
If you look at the world today where women are objectified, and regularly selected by physical beauty, the same was likely true in the past. But the only difference was that the dominant males probably had to be smarter to survive and breed. So you have a smart but ugly male with a dumb but beautiful female, the resulting child would likely be smart and attractive to some degree. Over time this intelligence has passed on to become mainstream, and while some may be smarter than others, some are more beautiful.



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09-11-02

Thine thoughts pertaining to evolution doth strike a chord within me which forces thy thoughts to remain constantly present. When thou speaks of mutations taking forever, one is remotely correct, for a mutation itself must be induced after some variable in the environment about the animal. Thou, however, does falter slightly when it pertains to thine own theory, which, while an interesting one, lacks enough evidence to back it. However, in the end, thou hast placed forth fine points, though thou must still battle against thy foes who are striking against thine theories.


Smack dab flat on my back,
The solid ground begins to crack,
I pulled her down and down and down,
I lost my breath I thought I'd drown.
Fistfuls of you, fistfuls of you,
You pulled me through with white knuckles,
White knuckles. White knuckles.)
Her leg, my hand, a smoldering brand,
Sticking to her wet body like sand,
Her place, distaste, we fell from grace,
Red smears across her face.


  
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09-11-02

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Thine thoughts pertaining to evolution doth strike a chord within me which forces thy thoughts to remain constantly present. When thou speaks of mutations taking forever, one is remotely correct, for a mutation itself must be induced after some variable in the environment about the animal. Thou, however, does falter slightly when it pertains to thine own theory, which, while an interesting one, lacks enough evidence to back it. However, in the end, thou hast placed forth fine points, though thou must still battle against thy foes who are striking against thine theories.
I'm sure you have the wrong thread, the "Your Irrelevant Opinion on the Value of Anothers Arguement" thread is somewhere else, this is Evolution Solved and requires at least some modicum of reasonable arguement which you can support, not just your foppish rambling.



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09-11-02

*Hugs the V-man*

One thing.. you said it isn't mutations, but evolution, then you start to use the term mutation in the next one pertaining to the alterations.

And nobody has yet to explain how exactly the human female managed to become altered correctly so that the baby would pop out early. (If you have, just point it out to me since I'm too tired at the moment to read everything).


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09-11-02

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Well.. according to this.. genes are made up of dna.. boy oh boy.. and I said that DNA isn't able to alter itself... and yet here you are saying that the genes are controlling the traits, and choosing what traits get passed on specifically, thereby allowing for a better creature in the end.
John, you have absolutely no idea what you're talking about. And you obviously won't look at any actual facts. Nor will you read what I say either. I never once said that the genes choose what gets passed on. Its merely a case of one aspect of a trait dominant over another.

I decided to show you an actual scientific report since you can't seem to do this on your own. This deals more with Gene-linked diseases, but it all works the same.

Quote:
Genetics is the branch of biology concerned with heredity and individual characteristics. Specific conditions and rare disorders may have a genetic basis. Where this is the case there will be a variety of causes. For example; the causes may include a single abnormal gene, a chromosomal abnormality or a genetic predisposition allied to other factors.

This section includes a glossary of genetic terms used throughout The Contact a Family Directory and it is written for the non-specialist. We shall concentrate mainly upon two forms of inheritance: the single abnormal gene and chromosomal abnormalities. Illustrations are used to explain certain patterns of inheritance.

The human body is made up of billions of cells. At the centre of each cell is a special compartment called the nucleus which stores threads of DNA (Deoxyribonucleic Acid) arranged in chromosomes. The chromosomes are in their turn composed of 50,000 to 100,000 genes which contain the genetic blue print determining each individual's characteristics.

The ovum and sperm each carry 23 chromosomes and on fertilisation the chromosomes combine to give a total of 23 pairs, 46 chromosomes in total. One pair of chromosomes determines the sex of the individual: males have an X and Y chromosome, while females have two X chromosomes.

Inheritance will depend upon the arrangement of the genes and the status mode of the gene: that is, autosomal dominant, autosomal recessive or X-linked recessive. (These terms are defined in the Genetics glossary).

1. SINGLE ABNORMAL GENE
A mutant (abnormal) gene is one where a gene may be considered as a variant of a 'normal' gene. This change may occur spontaneously by chance and have no significance for the individual concerned. In other cases, the gene which mutates (changes its character) may give rise to specific inherited disorders where there is no previous family history. Such a gene, in specific circumstances determined by status, can cause a specific disorder. Inheritance may be autosomal dominant, autosomal recessive or X-linked recessive.

More research has shown that in many conditions there may be different spelling mistakes or mutations in the gene which can cause the disease. For example, in cystic fibrosis over 200 different mutations can occur in the gene, but they mostly produce the same disease pattern.

AUTOSOMAL DOMINANT INHERITANCE
Autosomal means that males or females are equally affected. In dominant inheritance the chance of passing on the disorder is 50% for each pregnancy. If the gene is inherited it will result in an affected individual. Examples of such conditions are Huntington's Chorea or Tuberous Sclerosis. In some cases penetrance may not be complete in some individuals, resulting in a mild form of the condition. Sometimes the condition with autosomal dominant inheritance may arise due to a mutation in egg or sperm, and in such cases there would be no preceding history. This is illustrated in the diagram below.


AUTOSOMAL RECESSIVE INHERITANCE
In this form of inheritance the affected gene is recessive: two of the same gene mutations are required for the child to be affected by the disorder. In such cases the parents are unwitting carriers of the gene. The risk of an affected child being born will be 25% for each pregnancy. Examples of such conditions are Friedreich's Ataxia, Cystic Fibrosis or Phenylketonuria.

Unless the parents are related, the chances of marrying a carrier of the same recessive gene is low, though the incidence of the existence of recessive genes in the population varies with condition. Genetic counselling can help to predict the occurrence for individual families.


X-LINKED RECESSIVE INHERITANCE
This is a recessive form of inheritance where the mother carries the affected gene on the X chromosome. This means that girls are carriers and that usually only boys are affected by the disorder. Examples of such disorders are Duchenne Muscular Dystrophy, Haemophilia or Hunter Disease (a mucopolysaccharide disease).

Affected men will not pass the condition on to their sons but all their daughters will be carriers. This is because a man passes his Y chromosome on to his sons and his X chromosome to his daughters.

In some rare situations, female carriers may show mild features of an X-linked disorder, for example in Fragile X Syndrome


X-LINKED DOMINANT INHERITANCE
There are few examples of this type of inheritance, one such is Coffin-Lowry Syndrome. In this form males and females are both affected. An affected female will have a 50% chance of passing the disorder on to both her sons and her daughters. An affected male will pass the condition on to all his daughters, but not to his sons.


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09-11-02

This is an article I found on the university database, its very long so if your willing to take the time read it all the way through it is pretty thorough in its description of evolution and how it works.
Quote:
Molecular Evolution

--------------------------------------------------------------------------------
Accepted for publication:January 2000

Jan Klein Max Planck Institute for Biology, Tübingen, Germany

--------------------------------------------------------------------------------
Keywords: evolutionmolecular evolutiontaxonomygenealleleDNA

--------------------------------------------------------------------------------
Molecular evolution is the process by which molecules of living forms diverge from one another over time. The study of molecular evolution embraces the evolution of the molecules themselves, their origins, how they change from taxon to taxon, the effects of these changes on function, and the integration of the molecules in the biochemical pathways of an organism. It also infers phylogenetic relationships and contributes to the formulation of general principles of evolution at the molecular level.

--------------------------------------------------------------------------------
Introduction

For evolution to take place, changes must occur and they must then be handed on further. In the case of biological evolution, the changes (mutations) occur in the molecules of the hereditary (genetic) material, the nucleic acids, and their transmission from ancestor to descendant is guaranteed by the replication of these molecules. The changes may remain confined to the nucleic acids or they may be translated into an alteration of proteins encoded in the genetic material; the modified proteins may then effect the alteration of other molecules, sugars for example, and so on, until, at the end of the causal chain, changes affecting an observable character may take place. Ultimately, a molecular change in the genetic constitution (genotype) may thus be transliterated into altered appearance, physiology or behaviour – the organism’s phenotype. To become an evolutionary change, however, the mutation must spread through a group of individuals, the population. There are thus two principal levels at which evolution can be studied – the molecular and the population levels. Corresponding to a population at the molecular level is the gene pool – the total genetic material of an interbreeding population at a given time (in a more restricted sense, a gene pool is an assemblage of all alleles at a given locus in a population in a given generation; here a gene is a unit of inheritance, a sequence of nucleotides to which a specific function can be assigned; alternative forms of a gene are alleles and the position a gene or allele occupies on a chromosome is a locus). Evolutionary changes at the molecular level constitute molecular evolution. See also:Mutations and new variation: overview

The study of molecular evolution embraces three broad areas. First, it is concerned with the evolution of the molecules themselves, primarily sequences of nucleic acids and proteins – their origin, the manner in which they change from taxon to taxon, the effects of these changes on function, and the integration of the molecules in the biochemical pathways of an organism. Although almost any molecule or molecular segment can be selected for evolutionary analysis, certain molecules have become biologists’ favourites. These include haemoglobins, lysozymes, colour-sensitive pigment proteins, eye-lens crystallins, homeobox genes, and genes of the immune system such as those in the major histocompatibility complex (Mhc) and immunoglobulins. In a broader context, the study of molecular evolution also encompasses questions concerning life’s origin, the inception of life-sustaining molecules, and the emergence of fundamental life processes. This area of molecular evolution links up with molecular and cellular biology and with biochemical genetics. See also:Nucleic acids: general properties;Proteins: fundamental chemical properties;Regulatory genes in plant development (organ identity, homeobox, MADS);Major histocompatibility complex (MHC)

In the second area, the information on the molecules is used to infer phylogenetic relationships among organisms and to classify taxa. The relationships studied range from those among populations within a species to those among life’s domains and among the main branches of the ‘tree of life’. The selection of molecules (genes) to be studied depends on the degree of the expected relationship. For closely related taxa, microsatellites (short arrays of tandemly repeated basic units of DNA) and mitochondrial DNA are frequently used; for less closely related taxa, a wide range of molecules, including some of those listed above, is available; and for the most distant relationships, the choice falls on slowly evolving molecules such as ribosomal RNAs, transfer RNAs and heat-shock proteins, shared by all organisms. In this second area, the study of molecular evolution abuts on taxonomy and systematics. See also:Systematics 1800-2000;RNA structure;Chaperones, chaperonins and heat-shock proteins

The third area of molecular evolution is conceptual, aimed at the formulation of general principles of evolution at the molecular level. Here, researchers probe the nature of evolutionary change at the molecular level and its relationship to changes at the phenotypic level; they strive to identify the forces responsible for the changes, and seek to discover patterns in the evolutionary process. In this area, the study of molecular evolution stands on common ground with population genetics. See alsoopulation genetics: overview



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History

Molecules are not visible to the naked eye; although the large molecules of nucleic acids and proteins can be visualized with the aid of an electron microscope, the discernible detail is insufficient to spot changes in microstructure. The study of molecular evolution therefore only became possible after methods for detecting structural changes in macromolecules were developed. The first methods were indirect: they revealed that structural change occurred but provided no information about the nature of the change, nor about its location in the molecule. One indirect method took advantage of the immune system’s ability to distinguish foreign substances from those of the organism’s own. For example, the inoculation of human serum albumin into a rabbit leads to the production of antibodies, which react strongly with human, less strongly with chimpanzee and gorilla, and do not react with rhesus macaque serum albumin at all. This immunological reaction, which, if positive, results in the formation of a visible precipitate, indicates that human serum albumin is structurally somewhat different from the serum albumin of a chimpanzee or a gorilla, and quite distinct from the monkey protein. The ability of antibodies to differentiate between structurally distinct proteins and carbohydrates was already recognized at the turn of the century and was exploited in attempts to classify plants and animals. Later the method fell into disuse, only to be resurrected in the 1960s and 1970s. See also:History of taxonomy;Electron microscopy;Immunoprecipitation techniques

Three other methods – protein electrophoresis, DNA–DNA hybridization and restriction enzyme analysis – were also developed to detect differences between biological macromolecules without being able to ascertain the chemical nature of the changes. Electrophoresis distinguishes proteins according to their overall charge. DNA–DNA hybridization takes advantage of the observation that the two complementary strands of a DNA molecule dissociate (‘melt’) on heating and then reanneal again on cooling. If radioactively labelled, melted DNA of one species is mixed with melted DNA of another species and the mixture is cooled, the strands derived from the two species form hybrid duplexes. The extent of this DNA–DNA hybridization depends on the similarity of the DNA of the two species and it can be determined by heating the hybrid molecules: the greater the similarity, the higher the melting temperature of the hybrids. The third method puts to use restriction enzymes, proteins that have evolved in various bacteria as a means of providing protection from an invasion of foreign DNA. The enzymes attack the foreign DNA and hack it into pieces, each enzyme recognizing specific regions of the molecule. Because of the differences in structure, each DNA molecule yields a distinct set of fragments when digested with one or more restriction enzymes. The fragments can be separated and visualized, and their length can be determined by electrophoresis. See also:Restriction enzymes;Nucleic acids: hybridization

Ultimately, advances in biochemistry led to the development of direct methods by which the nature of mutational changes could be established. Biochemical investigations revealed proteins and nucleic acids to be strings of amino acid and nucleotide residues, respectively, arranged in a distinctive order. The methods enabled researchers to determine this order, or sequence, and to establish that it was different not only in distinct proteins or nucleic acids but also in the same proteins or nucleic acids of different species. Protein sequencing methods became available in the 1960s and, although they were later improved, they have remained laborious. Nucleic acid sequencing methods were developed some two decades later and quickly came into widespread use. Because a protein sequence can be deduced from a nucleic acid sequence and because nucleic acid sequencing is much simpler and faster than protein sequencing, the nucleic acid sequencing has now largely superseded protein sequencing in the study of molecular evolution. See also:History of biochemistry;DNA sequencing

Three other methodological developments contributed to the widespread use of nucleic acid sequences in the study of molecular evolution. First, the establishment of DNA cloning procedures solved both the problem of sorting out mixtures of molecules and that of obtaining pure populations of molecules. Second, the introduction of the polymerase chain reaction (PCR) technique provided a means of finding and amplifying a particular DNA fragment, even if it is present in the sample in a minute amount (in the most extreme case, in only one copy), and of finding homologous DNA segments in different, sometimes even extinct taxa. Third, the automation of the sequencing methods significantly shortened the time and effort required to determine the order of nucleotides in a nucleic acid. See alsoolymerase chain reaction (PCR)

The mass of sequence data would have become unmanageable, however, had statistical, computerized methods of sequence analysis not been developed. These methods enable evolutionary biologists to align sequences obtained from different taxa, to identify the similarities and differences, to infer the most probable relationships among the various sequences, and to assess the statistical significance of the relationships. See also:Molecular phylogeny reconstruction



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Principle

From the point of view of evolution, the simplest structural change (mutation) in a DNA molecule is the substitution of a nucleotide of one kind by another nucleotide during replication. The substitution may or may not effect a replacement of an amino acid residue in a protein, depending on the region and the site of its occurrence. A mutation generates a new allele that falls into one of three broad categories. An allele with the same chance of contributing its own copy to the next generation is said to be neutral. An allele that effects its own preferential transmission, increasing the chance of survival of its bearer or of producing a larger number of offspring (i.e. increases its fitness), is said to be selectively advantageous. Finally, an allele that decreases the chance of survival and reproduction of its bearer is considered to be selectively disadvantageous. See also:Mutations and the genetic code;Fitness

When a neutral mutation takes place in a population of Ne randomly breeding individuals, that is in a pool of 2Ne genes in a diploid organism, it constitutes one of 2Ne alleles. If every allele in the pool contributed one copy of itself to the next generation, the proportion of the mutant allele relative to all the other alleles (its frequency) would remain the same during the passage of generations. In reality, however, this never happens. By chance, some genes do indeed contribute their own copy, but others contribute more than one and others contribute none at all. The gene pool of each generation is then said to be produced by random sampling of the pool in the preceding generation. Because of the effects of random sampling, the frequency of a mutant allele may, again by chance, increase from one generation to the next, decrease, or stay the same. Chance fluctuation in allele frequency from generation to generation as a result of random sampling is referred to as random genetic drift. The most likely fate of a mutant allele is that it is lost from the pool; it becomes extinct within a few generations after its emergence. But from time to time a particularly ‘fortunate’ allele may increase in frequency over many generations until it replaces all other alleles in the pool – it becomes fixed. If each of the 2Ne alleles in the pool has the same probability of becoming fixed, the probability of fixation of the mutant gene is 1/(2Ne). The fixation rate, the probability of fixation of one of 2Nem mutations that occur every generation, is then equal to (2Nem)/(2Ne) = m, the mutation rate. The average interval between two successive fixations is 1/m. The average fixation time (i.e. the time required for a mutation destined for fixation to achieve a frequency of 1) is, for diploid organisms, 4Ne generations. See also:Mutations: origin, nature and impact;Drift: introduction;Variation: measures

Mutations occur constantly in all organisms. The great majority of them become extinct, regardless whether they are neutral or selectively advantageous (although the latter have a better chance of escaping elimination than the former), but from time to time one of them rises in frequency until it becomes fixed. (Selectively disadvantageous alleles are normally all eliminated.) Since there are many sites at which a mutation can occur in the DNA of each organism, the probability that two species will fix the same mutation is low. The fixation of distinct mutations leads to molecular divergence of species – their molecular evolution. The essence of evolution at the molecular level is, therefore, the differential fixation of mutations in distinct groups of organisms.



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Methods

Molecular evolution begins with allele-frequency changes in a population. To study these initial changes, researchers sample a population and test all individuals in the sample for the presence of variants of a particular molecule. The tests reveal different frequencies of alleles at a given locus in the population – polymorphism. In the case of neutral alleles, polymorphism amounts to a snapshot of the ascendancy–descendancy process. For certain types of advantageous alleles, polymorphism may be the result of a balance between the effects of a selective advantage of one allele relative to that of another. The balance may maintain alleles in a population at relatively stable frequencies over long time periods. Both neutral and balanced polymorphisms may be passed on to new species when these arise by the splitting of an ancestral species (trans-species polymorphism). The choice of methods for the study of polymorphism is influenced by the necessity of testing large sample sizes. The methods commonly used include special modifications of the electrophoresis technique, a combination of PCR with restriction enzyme analysis, and sophisticated immunological techniques. See also:Molecular polymorphism: amounts;Restriction enzymes

Information about the fixed differences between taxa is obtained by comparing their nucleotide sequences. It can be expected that nucleic acid or protein sequences of more closely related species will reveal a greater similarity to one another than sequences of more distantly related organisms. Sequences can therefore be used to infer evolutionary or phylogenetic relationships among taxa. To make such inferences, a researcher first aligns the sequences by arranging them into rows in such a way that at each site (position), the residues of the different sequences are in a single column. Often alignments are only made possible when gaps are artificially introduced into the sequences; these presumably correspond to insertions or deletions (indels) of residues undergone during the evolution of the molecule. See alsoNA sequencing

There are two principal methods for inferring phylogenetic relationships from aligned sequences. First, the relationship can be assessed on the basis of the genetic (evolutionary) distance between the sequences: the larger the distance, the less related are the sequences and the organisms. Genetic distance is obtained by dividing the number of observed differences between two sequences by the total number of sites (positions) compared. In these comparisons, however, the possibility that, at some sites, identity may have arisen although there was a difference in an intermediate, or that the observed difference has arisen in more than one step, must be taken into account. In both instances, the number of changes that actually occurred during evolution would be greater than that indicated by the observed differences. However, the probability of these hidden changes occurring can be assessed and the actual distances can be estimated. The sequences can then be clustered by placing those separated by smaller distances closer together than those separated by larger ones. The result is a phylogenetic tree that is presumed to reflect the evolutionary relationships among the sequences. See alsohylogeny reconstruction

The second method strives to reconstruct the succession of changes that led to the observed sequence differences. The reconstruction is guided by the principle of parsimony, which assumes that if multiple paths could theoretically lead to the same state, the one taken by evolution is that requiring the smallest number of evolutionary changes. The justification for the use of this principle is that since the changes are rare, the probability of multiple hits at the same site is lower than that of a single change. The path obtained by this maximum parsimony method, too, is expressed in the form of a phylogenetic tree. To obtain the most parsimonious tree, the researcher ideally considers all theoretically possible pathways that could yield the observed sequence differences and then selects the one requiring the fewest changes along the way.

Both distance and parsimony methods exist in many versions. Various computer programs have been designed to enable a tree to be drawn from the aligned sequences; indeed, the alignment of sequences itself has also been computerized. A single molecule-based tree, however, may not accurately reflect the evolutionary history of the organisms from which the molecules have been isolated: the gene tree may differ from the species tree. There are numerous complicating factors that may be responsible for the incongruence. One of them is trans-species polymorphism and the ultimate differential fixation of the polymorphic genes in the descendant species. Another is the inaccuracy associated with attempts to estimate the true number of changes at individual sites. Inferences that are made regarding the relationships of species must therefore be based on the examination of several genes or proteins.



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Molecular Clock

Phenotypic evolutionary changes are highly erratic. Some lineages may change rapidly within a short time, while others appear not to have changed their phenotypes for many millions of years. Early protein sequence comparisons suggested that, at the molecular level, amino acid replacements might accumulate at a much more regular pace. Indeed, if a large proportion of nondeleterious mutations were neutral in terms of their effect on fitness, their fate in the gene pool would be determined by random genetic drift and fixations could be expected to occur at more or less regular intervals. It would, however, be a stochastic regularity, rather like that leading to the expectation of obtaining 50% heads in coin flipping: the more times you flip a coin, the closer the match between the observed and the expected result. The supposition that molecules evolve at an approximately constant rate is termed the molecular clock. According to the molecular clock hypothesis, the number of amino acid replacements (and by extension also the number of nucleotide substitutions) found between proteins (nucleic acid segments) of two species is proportional to the time elapsed since the divergence of these species from their common ancestor. If the hypothesis holds true, it should be possible to use proteins and nucleic acids for determining not only relations