Comment on How much of the Human Genome is Functional? by Sean Pitman.
It was my understanding that we were discussing the human genome, not the bacterial genome.
It doesn’t matter. The principles are the same.
Obviously, humans have been tinkering with the bacterial genomes for a long time, and made some fascinating discoveries. Humans are now tinkering with the human genome, but generally for the correction of harmful mutations. Even if humans should be successful in improving the human genome over its normal state (and that is a big “if”), this is no proof of naturally occuring evolutionary improvements.
While detrimental mutations do vastly outnumber beneficial mutations, the fact is that beneficial mutations do occur – even in humans. Here are a few examples:
1) The ccr5-Δ32 mutation confers HIV-1 resistance (as well as resistance to plague and smallpox) to those with a double copy of the allele (homozygous). (Link)
2) A small community in Italy is known to have a mutant version of this protein, named Apolipoprotein AI-Milano, or Apo-AIM for short. Apo-AIM is even more effective than Apo-AI at removing cholesterol from cells and dissolving arterial plaques, and additionally functions as an antioxidant, preventing some of the damage from inflammation that normally occurs in arteriosclerosis. People with the Apo-AIM gene have significantly lower levels of risk than the general population for heart attack and stroke, and pharmaceutical companies are looking into marketing an artificial version of the protein as a cardioprotective drug. (Link)
3) There are also drugs in the pipeline based on a different mutation, in a gene called PCSK9, which has a similar effect. People with this mutation have as much as an 88% lower risk of heart disease. (Link)
4) Another beneficial mutation was first discovered when a young person from a Midwest family was in a serious car crash from which they walked away with no broken bones. X-rays found that they, as well as other members of the same family, had bones significantly stronger and denser than average. One doctor who’s studied the condition said, “None of those people, ranging in age from 3 to 93, had ever had a broken bone.” In fact, they seem resistant not just to injury, but to normal age-related skeletal degeneration. (Link)
5) There have also been mutations to human mtDNA that allows people in cold weather environments to survive better than those who don’t have these particular mutation. (Link)
And the list goes on and on…
Research on E. Coli bacteria, where one can observe billions of organisms over a short period of time, is much different from genetic research on the human genome. Whether or not bacteria can modify mechanisms of processing lactose or citrate, or develop alternate pathways inducing antibiotic resistance is, in my opinion, hardly evolutionary. These simple bacteria will always be bacteria, and are certainly not evolving into higher organisms. They are simply improving their survival.
That is the very definition of “evolution” via random mutations and function-based selection that favor survival in various environments. The reason why these bacteria “will always be bacteria” is because of the limits of what the evolutionary mechanism can do when it comes to “levels of functional complexity”. Evolution only works on the lowest rungs of the ladder of functional complexity – i.e., no higher than systems requiring 1000 specifically arranged amino acid residues.
This, in fact, is hardly a good thing for humans. It would be much preferable for humans to mutate and produce mechanisms of bacterial destruction. If some humans would mutate a gene that would selectively destroy harmful bacteria, that would be quite an event!
That already happens. It’s called immunity. Vaccinations, for example, help the immune system “learn” which bacterial and viral antigens to attack in the future…
While on the subject of lactase evolution, it should be noted that many humans have mutated into a state of lactase deficiency, thereby being unable to process lactose efficiently. Many of these humans are miserable when consuming dairy products. I think we would hardly label this a positive mutation, although this type of mutation is not nearly as harmful as cancer-producing mutations, or so many other life-shortening mutations.
Again, everyone agrees that detrimental mutations are far more common than beneficial mutations.
I am still extremely interested in any observed naturally occuring mutation in the human genome which has been found to be beneficial.
Well, now you know…
Sean Pitman Also Commented
How much of the Human Genome is Functional?
Good response.
How much of the Human Genome is Functional?
You do realize that I’m not a neo-Darwinist? The evolutionary mechanism of random genetic mutations and natural selection is limited to the lowest levels of functional complexity. It cannot produce any qualitatively novel system that requires more than 1000 specifically arranged amino acid residues this side of trillions upon trillions of years of time (Link). It’s a statistical problem due to the nature of sequence space at higher and higher levels of functional complexity…
How much of the Human Genome is Functional?
@dana:
Prions are interesting. However, prions don’t really self-replicate themselves starting with random amino acids. Usually the same amino-acid residue sequence is required to already exist in a pre-formed protein before this pre-existing protein can then acquire the 3D prion conformation. The prion simply refolds the pre-existing protein with the same or similar sequence into a new conformational shape.
This isn’t like a self-replicating organism where randomly arranged nucleic acid molecules are specifically sequenced by protein-based machinery based on a pre-existing DNA sequence template. In other words, the way prions works is not like replicating a complex mechanical machine from scratch – from a pile of fundamental building blocks.
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