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My response to David

Response to Point 5

Hello Jeff,

Thanks for getting back to me. The following is an essay that I recently wrote in response to this issue. As I'm sure you're aware, the theory of evolution suggest that very drastic changes, such as developing the ability to fly, occur over many millions of years. However, concrete examples of entirely new biological pathways (see the example of Cit+ E. coli below) have been demonstrated in the laboratory in less than one human lifetime. These concrete examples provide a specific location on the genome and even the specific mutation responsible for the new mutant allele. When one extrapolates these examples over many millions of years, and especially when one considers the fossil record as science already knows it, it's not difficult to imagine macroevolutionary processes creating eyes, wings, or echolocation.

Microevolution is a process that results in the gradual change of a species through evolutionary processes over a very large period of time. It has been suggested by opponents of the theory of evolution that microevolution only selects from pre-existing variation in the population and that mutation is not a source for new variation in a population. This concept of microevolution works to disprove the evolutionary theory by suggesting that the genetic code responsible for all of the variation we see in life already exists in the genome and that microevolution does nothing more than exert a new selection pressure, exposing those variations. This opposing concept claims that genetic mutation cannot be responsible for beneficial mutations thereby indicating that a novel genome cannot change over time. However, the claim that microevolution cannot act on mutation to create variation in a population is falsifiable by empirical reasoning as well as a number of different experiments to include Esther and Joshua Lederberg’s work with Escherichia coli, Richard Lenski’s work with Escherichia coli¸ and Dallas M. Swallow’s analysis of lactase persistence in Humans. Clearly, ample evidence exists to show that genetic mutation is a viable origin of variation for microevolution to act upon.

Microevolution is a process that changes the genome of a species without the occurrence of a speciation event; that is to say, microevolution represents relatively small changes to allele frequencies of a given species population that do not result in the derivation of a new species. Microevolution encompasses the demonstrable processes of natural selection, genetic drift, mutation, migration, and assortative mating. Of these five processes, mutation is the only one capable of producing new genotypes; the other four are mechanisms to change allele frequency. Extrapolating upon this idea that mutation is the only process capable of creating new variation and that natural selection works to destroy variation, we would expect to see no variation in populations if mutation was not occurring but natural selection was. Clearly this does not occur.

Conversely, given a population that is not undergoing microevolutionary change, we would expect to see new variation and allele frequency change if a mutation does occur. New variation is witnessed in stable populations after the occurrence of mutation events, demonstrating the mutations do lead to new variation. Indeed, experiments by Luria and Delbruck with E. coli have demonstrated a mutation rate of 1 mutation per 300 chromosome replications. Using this information, higher order eukaryotes with multiple chromosomes can be expected to produce one mutation per genome per generation (Maloy, 2004)! Furthermore, when one considers bacterial or insect resistance to antibiotics and pesticides the amount of genotypic variability that would have to be present in a population to allow it to adapt to any number of artificially created killing agents is statistically impossible. It seems highly unlikely that all of the resistance we see in bacteria and insects to man-made chemicals that do not resemble any naturally occurring compounds has always been present in these organisms. To refute this concept that organisms already contain all of the genetic material necessary to produce the variability of life we see today, it follows that demonstrable mutations must occur at observable and distinct places on the genome and that scientists should be able to pinpoint when these changes occur. Indeed, several experiments have done just that. Joshua and Esther Ledenberg sought to demonstrate that mutation occurs randomly in a population and not as a result of environmental selection pressure. In their 1952 experiment, a single bacterial genome was used to produce several different bacterial colonies. The colonies then were stamped onto a media containing penicillin where most colonies died, but some persisted. These colonies had developed resistance to the penicillin. In order to demonstrate that this resistance was present in the same colonies on the original plate and did not arise after the bacteria were exposed to penicillin; the original plate was washed with penicillin. As expected, the same colonies that survived when transferred to the plate containing penicillin also survived when the original plate was washed with penicillin (Berkeley Evolution, 2006). From this empirical observation, one can infer that the mutation did not occur in response to the new media and that it was present in the population on the original plate. However, because all colonies resulted from one original bacterial genome, variation through mutation must have occurred because some of the resulting genetically unique colonies developed penicillin resistance while some did not. It is irrelevant if the original bacterial genome was resistant to penicillin, what is important is that after several subsequent generations, some of the original bacterial genome’s progeny were resistant and some weren’t. Observations such as this are commonplace in science today and we are now able to pinpoint the location of mutations which cause such variation on the genome.

In modern humans, a mutation in the LCT gene on chromosome 2 allows some people to digest lactase into adulthood. Lactase persistence is widely seen in Caucasian populations and some dairy farming African tribes. It is believed that the mutation to the LCT gene which formed LCT*P, the mutated gene responsible for lactase persistence in modern humans, occurred between 9 and 6 thousand years ago; around the time early humans first domesticated cattle and began to practice milk based pastoralism. The genetic basis for lactase persistence is demonstrated by the high correlation of lactase persistence with race. Additionally, studies by Dallas Swallow show familial inheritance of lactase persistence as well as intermediate lactase persistence in heterozygotes for the lactase persistence allele. These heterozygotes are nearly phenotypically identical to homozygotes for LCT*P because the amount of lactase produced is usually sufficient to digest substantial amounts of lactose. It is only when heterozygotes consume huge quantities or lactose or are exposed to stress that they are unable to digest lactose sufficiently. Clearly, there is a very direct genetic, heritable, basis for lactase persistence in humans. By studying patients who do exhibit lactase persistence and comparing their LCT gene to people who do not exhibit lactase persistence, Swallow was able determine that 11 single nucleotide polymorphisms exist for the LCT gene. However, it appears that one substitution in particular is responsible for lactase persistence. Swallow concluded that a single nucleotide polymorphism that occurs upstream from the start of transcription for the LCT gene is responsible for almost all cases of lactase persistence in Humans (Swallow, 2003). A single nucleotide substitution determines lactose intolerance or lactase persistence in Humans! The specific location of this mutation is known, however, this study could not be replicated in a lab.

The Long Term Evolution Experiment was founded in 1988 by Richard E. Lenski. In this experiment, twelve identical populations of Escherichia coli were grown on a glucose-limited medium which also contained citrate. Under normal aerobic conditions, E. coli is not capable of using citrate as a carbon source. Every 500 generations, a sample of each population was frozen to keep a “fossil record” of E. coli’s evolution throughout the experiment. None of the twelve populations evolved the ability to utilize the citrate after > 30,000 generations. Finally, after 31,500 generations a citrate-using variant (Cit+) appeared. Over the course of the Long Term Evolution Experiment, each population experienced billions of mutations, more than the 4.6 million base pair genome. This suggests that every typical one step mutation had occurred in each population and that the mutation to evolve Cit+ must have been extremely rare. It is likely that Cit+ depends upon one or more earlier mutations, meaning that the emergence of a citrate-using variant depended heavily on each population’s unique mutational history. Although the Cit+ variant appeared at 31,500 generations, it did not become the dominant until between generations 33,000 and 33,500. This suggests that the first Cit+ variant, while capable of utilizing citrate, was not very efficient. In subsequent generations, through one or more mutations between generations 33,000 and 33,500, citrate utilization was greatly improved and resulted in a Cit+ population explosion. The result of further experiments conclude that the genetic background of later generations in Cit+ populations contributed to the increased potential to evolve the extremely rare Cit+ phenotype (Lenski, Borland, & Blount, 2008). The Long Term Evolution Experiment demonstrates an example of microevolution witnessed by the Human eye in less than one lifetime. Lenski has been able to point to specific genes likely to hold the mutations responsible for the emergence of Cit+ as well as demonstrate a complex mutant phenotype variant arising from several contingent genotype mutations.

Clearly, mutation is a causative agent of microevolution and the only source of new variation in a given population. Empirical reasoning disproves the notion that new genetic variation does not occur. Additionally, countless scientific studies demonstrate that new variation does occur and can often point directly to the nucleotide base pair responsible for the mutation and the time frame in which this mutation that lead to a new variation occurred. Empirical reasoning and scientific study seem to make the theory that mutations cause new variation in populations irrefutable.

 

David Ince
davidince08@gmail.com

 

Works Cited

Berkeley Evolution. (2006). The Lederberg Experiment. Retrieved May 5, 2011, from http://evolution.berkeley.edu/evosite/evo101/IIIC1bLederberg.shtml

Lenski, R. E., Borland, C. Z., & Blount, Z. D. (2008). Historical contingency and the evolution of a key innovation in experimental population of Escherichia coli. National Academy of Sciences, 7899-7906.

Maloy, S. (2004, July 10). Mutation Rates. Retrieved May 5, 2011, from San Diego State University College of Sciences: http://www.sci.sdsu.edu/~smaloy/MicrobialGenetics/topics/mutations/fluctuation.html

Swallow, D. M. (2003). Genetics of Lactase Persistance and Lactose Intolerance. Review in Advance, 197-219.