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Mutation and Evolution

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Mutation and Evolution Empty Mutation and Evolution

Post by admin @ shivam on Sat Jan 10, 2009 8:38 pm

Mutations are the raw materials of evolution.

Evolution absolutely depends on mutations because this is the only way that new alleles are created.
But this seems paradoxical because

* most mutations that we observe are
o harmful (e.g., many missense mutations) or, at best,
o neutral, for example:
+ "silent" mutations encoding the same amino acid
+ many mutations in noncoding DNA (e.g. "junk" DNA).
* most mutations affect a single protein product (or a small set of related proteins produced by alternative splicing of a single gene transcript) while much evolutionary change involves myriad structural and functional changes in the phenotype.

So how can the small changes in genes caused by mutations, especially single-base substitutions ("point mutations"), lead to the large changes that distinguish one species from another?
These questions have, as yet, only tentative answers.
The Problem of Harmful Mutations
One Solution: Duplication of Genes and Genomes

Mutations that would be harmful in a single pair of genes can be tolerated if those genes have first been duplicated.

Gene duplication in a diploid organism provides a second pair of genes so that one pair can be safely mutated and tested in various combinations while the essential functions of the parent pair are kept intact.

Possible benefits:

* Over time, one of the duplicates can acquire a new function. This can provide the basis for adaptive evolution.
* But even while two paralogous genes are still similar in sequence and function, their existence provides redundancy ("belt and suspenders"). This may be a major reason why knocking out genes in yeast, "knockout mice", etc. so often has such a mild effect on the phenotype. The function of the knocked out gene can be taken over by a paralog.
* After gene duplication, random loss of these genes at a later time in one group of descendants different from the loss in another group could provide a barrier (a "post-zygotic isolating mechanism") to their interbreeding. Such a barrier could cause speciation: the evolution of two different species from a single ancestral species.


* Paralogous genes. Genes in one species that have arisen by duplication of an ancestral gene. Example: genes encoding olfactory receptors.
* Duplication of the entire genome. Examples:
o Polyploid angiosperms.
o Genome analysis of three ascomycetes show that early in the evolution of the budding yeast, Saccharomyces cerevisiae, its entire genome was duplicated. Each chromosome of the other ascomycetes contains stretches of genes whose orthologs are distributed over two Saccharomyces cerevisiae chromosomes.
o There is also evidence that vertebrate evolution has involved at least two duplications of the entire genome. Example: both the invertebrate Drosophila and the invertebrate chordate Amphioxus contain a single HOX gene cluster while mice and humans have four. [View]

A Second Solution: Mutations in Regulatory Regions
Not all genes need to be expressed in all cells. In which cells and when a given gene will be expressed is controlled by the interaction of;

* extracellular signals turning on (or off)
* transcription factors, which turn on (or off)
* particular genes

A mutation that would be lethal in the protein coding region of a gene need not be if it occurs in a control region (e.g. promoters and/or enhancers) of that gene.
In fact, there is increasing evidence that mutations in control regions have played an important part in evolution. Examples:

* Humans have a gene (LCT) encoding lactase; the enzyme that digests lactose (e.g. in milk). In most of the world's people, LCT is active in children but is turned off in adults. However, northern Europeans and some other people for whom milk remains a part of the adult diet carry a mutation in the control region of their lactase gene that permits it to be expressed in adults — an example of a polymorphism.
* There are very few differences in the coding sequences between genes of humans and chimpanzees. However, many of their shared genes differ in their control regions.
* The story of Prx1. Prx1 encodes a transcription factor that is essential for forelimb growth in mammals. When mice have the enhancer region of their Prx1 replaced with the enhancer region of Prx1 from a bat (whose front limbs are wings), the front legs of resulting mice are 6% longer than normal. Here, then is a morphological change not driven by a change in the Prx1 protein but by a change in the expression of its gene.

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