Sunday, March 29, 2009
Speed of evolution
Mr. Carroll makes it clear that natural selection happens gradually. Mutations occur randomly, and when they do occur it takes many generations to spread over the entire population. However, it is also clear that some mutations work their way into the population relatively quick. On page 56, he wrote that the development of armor plating in stickleback fish was "rapid". What determines the quickness of a mutation? Does the species it is occurring in matter? Does the mutation itself matter? Discuss generation times, different species, effectiveness of mutations, etc.
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Mutations occur through errors during cell division. It therefore makes sense that species with shorter generation times evolve faster because reproduction and cell division occur more often. It has also been noticed that mutations tend to be more common in males because their germ cells undergo more divisions as opposed to females. An average human male can produce around 85 million sperm per testicle per day as opposed to a female who is born with only one to two million oocytes and never produces any more. This leaves the male with a much greater chance for mutation because cell division is occurring continually at such a rapid rate.
ReplyDeleteAs far as whether or not the mutations actually make their way into the genetic makeup of the species over time, that is left to natural selection. Mutations are all random and they occur by complete accident. Some mutations can be good while others can be bad and most have no effect at all. If a mutation somehow gives the species a selective advantage, such as the armor plating in the stickleback fish, it may make its way into the population as it is passed on through the generations and those individuals with the new trait have a better chance at survival. However, just because a mutation may result in a selective advantage does not mean that it will become a prevalent trait in the population. Often, these traits are lost before they make their way into the population as they are not successfully passed on through the generations. Mutations that result in a disadvantage are eliminated as individuals with those traits are not as successful and do not pass their genes on.
In Carroll’s discussion of selection, time, and mutations he explains how mutations are continual phenomenon in society: “evolution is an ongoing process” (65). The spread of mutations, Carroll summarizes depends on factors such as numbers of sites per genes, the number of genes per organism, the number of mutations per site, population size, and birth rate. In addition, Carroll recognizes that although there may be many mutations that occur, not all of these mutations express themselves because later on in time natural selection may reject such a mutation or fossilize such a mutation, rendering it nonfunctional.
ReplyDeleteAs Katie has already mentioned, one of the main sources of mutations is cell division. There are several steps in the cell cycle that are prone to mutation during meiosis. For example in meiosis I, mutations can occur in the process of crossing over. During the process of crossing-over one of the paired chromosome arms may exchanged physically at one or more locations. If the two chromosomes contain different mutations on each side of the cross-over the exchange of chromosome arms will produce chromosomes that contain different combinations of mutations.
The Double-Stranded-Break Repair Model ,conceived in 1983 at the University of Oregon by Frank, explains the process of crossing-over. First a break within one of the two homologous chromosomes caused by the synaptonemal complex which the homologous chromosomes are lined up next to each other. A gap is created by enzymes that chew the break. One of the ends uncoils and attaches itself with the other undamaged strand that has a mirror nucleotide combination. A single strand loop is created by the undamaged strand. The broken strand begins to grow in the undamaged one, adding new nucleotides on the ends based on the undamaged strand's nucleotides. The loop continues to get larger due to this growth. The growth fills up the gap made by the enzymes and at the same time, the used broken strand also fills in the gap. The damaged ends are sealed by other enzymes, making the two pairs that are continuous. However one strand from each pair has exchanged segments with the other in two places. Finally the crossed-over strands break apart, removing the bridges between the two homologous chromosomes, and thus we have mutations.
In addition to the mutations causes by crossing-over, the rate of mutations can also be influenced by genetic drift: “the random nature of transmitting alleles from one generation to the next given that only a fraction of all possible zygotes become mature adults” (Moran). The rate/impact of genetic drift is most concentrated in small populations. For example, if a pair of diploid sexually reproducing parents have only a small number of offspring then not all of the parent's alleles will be passed on to their offspring because of the chance assortment of chromosomes. In a large population this will not have much effect in each generation because the random nature of the process will tend to average out. But in a small population the effect could be prominent.
Thus in humans the most effective way to experience mutations is probably through the process of genetic drift, more specifically the founder effect, or when a small group breaks off from a larger population and forms a new population. The founder effect is probably responsible for the lack of blood group B in American Indians, whose ancestors arrived in very small numbers across the Bering Strait about 10,000 years ago.
The most basic break in the rate of mutations according to species is in terms of type of reproduction: asexual vs. sexual species. The fact that a gene is passed to all the offspring of an asexual individual and to only half the offspring of a sexually reproducing individual provides a 2-fold fitness advantage to a new mutation that confers asexual reproduction when it arises in a population of sexual organisms. This 2-fold difference in fitness is known as the “2-fold cost of meiosis”
Individuals in poor physiological condition have higher mutation rates. Assuring the fidelity of DNA replication is metabolically costly and involves the products of many dozens or hundreds of genes. Individuals in poor condition will have fewer resources to devote to genomic surveillance, leading to the possibility that individuals in poor condition will suffer an increased mutation rate.
In an experiment conducted with 5 different genome comparisons -primates, rodents, fruit fly, rice and yeast- the experiment demonstrated that the rate of single nucleotide mutations, or nucleotide divergence, increases near indels (insertions/deletions) in the gene. Thus, one explanation of mutation rates ( a sort of positive feedback of one broader mutation tuning a more minute mutation) is that heterozygosity for an indel is mutagenic to surrounding sequences.
There are now artificial means by which to purge a harmful mutation from a population. Let’s say a certain mutation in a flower causes the petals to whiter more rapidly, scientists can harness the power of natural selection and reject this injurious mutation by using RNAi. RNAi is a system within living cells that helps to control what genes are active and how active they are. The process uses micro RNA and siRNA. It is initiated by the enzyme Dicer, which cleaves long double-stranded RNA molecules into short fragments of ~20 nucleotides. One of the two strands of each fragment, known as the guide strand, is then incorporated into the RNA-induced silencing complex (RISC). This leads to post-transcriptional gene silencing, which occurs when the guide strand base pairs with a complementary sequence of a messenger RNA molecule and induces cleavage by Argonaute, the catalytic component of the RISC complex. Thus, scientists can now try to induce this process to purge a population of harmful DNA. However, the power of natural selection should by cautiously wielded by man.
Sources:
http://www.talkorigins.org/faqs/genetic-drift.html
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2253642
http://www.nature.com/nature/journal/v437/n7055/full/nature04072.html