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Debate: 15 questions for evolutionists (view source)
Revision as of 21:40, January 25, 2012
, 21:40, January 25, 2012→What an evolutionist would say
When natural selection is added to the equation, there is a mechanism by which good mutations can be screened from bad ones, and a mechanism for gene frequencies to change in a way that allows a species to slowly adapt to their environment. Not all mutations are beneficial, obviously, but the environment punishes bad DNA very quickly, and after billions of years life has become very sophisticated, even on the smallest scales.[[User:TonyPark|TonyPark]] 12:18, 13 January 2012 (EST)
When natural selection is added to the equation, there is a mechanism by which good mutations can be screened from bad ones, and a mechanism for gene frequencies to change in a way that allows a species to slowly adapt to their environment. Not all mutations are beneficial, obviously, but the environment punishes bad DNA very quickly, and after billions of years life has become very sophisticated, even on the smallest scales.[[User:TonyPark|TonyPark]] 12:18, 13 January 2012 (EST)
::Yet another very well-worded answer. Mr. Park, you are a tough act to follow!
::Seriously, what is the deal with the creationist obsession with mutating genes? Seriously, the idea that changing the genes is a major driving force of evolution pre-dates the understanding of how genes work. There are plenty of other ('''much''' more common and interesting) ways to generate phenotypic variation within a population. In the past three decades, advances in population genetics, combined with a veritable revolution in the fields of molecular biology and developmental biology, have demonstrated that. In other words, referencing the breakthroughs that have resulted from the new-found understanding of the molecular mechanisms of evolution, '''"This ain't your daddy's Darwin!"'''
::But first, because the question insists, I will address the boring stuff.
::Genes duplicate, entire sections of chromosomes, and sometimes even whole chromosomes, or sets of chromosomes, can be duplicated or even fused. Sometimes, just a portion of a gene is duplicated, or maybe even swapped with a part from a different gene. On a smaller scale, errors in DNA replication, among other factors, can cause single base pairs in DNA to be changed (this is called a "single nucleotide polymorphism" or a SNP--pronounced "Snip"), deleted, or inserted. Sometimes, it's a transposable element (chunks of DNA that like to move around in the genome--a lot) that inserts in the middle of an exon. Or maybe even an endogenous retrovirus that's still intact enough to move around finding itself in between two enhancer elements for an essential gene. Chromosomes are not static structures either. High school biology was only partially right when they taught you that recombination occurs between homologous chromosomes during meiosis; as it turns out, non-homologous chromosomes trade parts too sometimes (quite often, actually, on an evolutionary time scale). In short, on the scale of hundreds of millions of years, the genome has more in common with Mardis Gras in New Orleans than it does with a leather-bound book. To call mutations "accidents", overlooks how commonly they occur on evolutionary time scales.
::On the genomic level, when and where mutations occur is largely random. The vast majority of mutations have no effect whatsoever on phenotype. However, when a mutation does affect phenotype, whether or not it survives to be present in future populations is not random. Any genomic change that increases an organism's ability to reproduce efficiently, will gradually become increasingly prevalent in subsequent generations because the more-efficiently reproducing individuals generate more offspring. Alternatively, if a variation impairs the ability of an individual to reproduce efficiently, then that variation will become less prevalent in subsequent generations because the individuals carrying it will produce proportionately fewer offspring. This seemingly obvious observation '''is''' natural selection. To say that a trait is "selected against" simply means that it has a deleterious effect on the relative reproductive potential of the individuals carrying it.
::Random mutations generate novel allelic variations within a population, and the sieve of reproduction keeps the randomly-occurring harmful variations from being present in future populations while at the same time amplifying the number of individuals carrying favorable variations. The net result of this process is anything but random.
::That said, ecosystems change, natural disasters happen, geological events happen, new organisms colonize an ecosystem and disrupt the food chain. An allele that was beneficial in one generation, may be quite deleterious four generations later. But, when that happens, selective pressure shifts and individuals carrying the now-harmful allele are out-reproduced by individuals who are better adapted to the new conditions--thus the allelic composition of the population shifts again. Repeating a similar cycle over hundreds of generations will result in a population that is, by and large, phenotypically different (sometimes quite dramatically) from the original population. Repeat the cycle over tens of thousands, or hundreds of thousands, or millions, of generations, and add in a whole host of other possible random events that favor or cause a redistribution of allele frequencies over the generations, and the end population will have changed drastically from the original population.
::Now for the fun stuff. The regions of important genes that encode for important proteins are under quite a bit of selective pressure to change as little as possible over the generations; a random mutation in one those regions would be so harmful to the reproductive ability of the individuals carrying it that it is not likely to persist in a population for more than a few generations (assuming it's not lethal to the original carrier, in which case it would not even be present in one). As such, mutations in functional protein coding genes are not a major driving force of phenotypic change across generations. This is why the fruit fly makes a good model for human genetics--the superfluous regions of the genes (that, say, encode for parts of proteins where the amino acid sequence is largely inconsequential) have diverged quite a bit, but the important parts have stayed the same over the hundreds of millions of years since the last common ancestor between the fruit fly and the human. They have retained this "homology" because any changes in those regions was very strongly selected against.
::So what is the major cause of morphological change? Among closely related species (and, yes, for the purpose of this explanation humans are '''very''' closely related to mice), the major genetic differences underlying morphological variation are not in the protein-coding regions of the genes themselves, but in the promoter (regulatory) regions of these genes. Mutating an essential component gene that is essential to normal embryonic development is going to result in a dead embryo--not a reproductively viable organism. However, subtly adjusting the "on/off" switch of such a gene, and tweaking its expression pattern (which cells express a given gene), will both allow the organism to grow to reproductive viability, and produce a morphological change. If individuals with this new morphological change are able reproduce more efficiently than individuals without it, it will become increasingly prevalent in future generations.
::As for how new genetic information is added (by which, I assume, you mean the emergence of new protein-coding genes), we return to the hustle and bustle of the chromosomes. Gene duplication events are very common. When an organism only has one or two (depending on the nature of the gene and the mutation) copies of an important gene to play with, significant changes will be very strongly selected against. When a gene is randomly duplicated, the organism now has a spare copy--and may accrue mutations in one of the copies of that gene without seriously impacting its reproductive potential. As mutations accumulate in the copy of the gene that is now freed from negative selective pressure, it will most likely just wind up as a useless (junk) sequence in the genomic junkyard (there are thousands of such non-functional duplicate-gene remnants in the human genome). If, however, as its sequence diverges from that of its "functional" copy, its mechanical function (or expression pattern, or both) changes in such a way that it provides a survival benefit to the organism carrying it, individuals carrying the divergent copy (now a new gene in its own right) will be selected for in subsequent generations and progressively more beneficial allelic variations of the new gene will be selected for.
::Similarly, when a large segment of a chromosome is duplicated, every new duplicate gene contained in that segment is entered into the "new gene lottery", for a chance to become new (repurposed) genetic information. This too is a fairly common occurrence, especially when there is a lot of selective pressure for novel adaptation.
::Evolution has been a '''long''' road. It's taken 4 billion years for gene duplication, sequence divergence, random catastrophes, population events, and the cut-throat race for reproductive viability to lead to life as we know it today.
===What a creationist would reply===
===What a creationist would reply===