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Smidlee said:
highwaystar101 said:
 

 

2. Well, you can see the need for developing new treatments to combat bacteria becoming resistant to our drugs however you want. But how about the transformation of acidophobe to acidophile of e-coli? That is a huge evolution, especially for 40,000 generations in a shorter time scale with an evolution much larger than just becoming drug resistant.

 


I thought I read something these e-coli has loss some of it's ability to repair it's DNA so they couldn't survive outside the lab. This is like winning a million dollar  in a lottery after you bought 10 million dollars of tickets. If this is huge evolution it seems to be a huge loss.

Actually that was just a mid-step process that allowed them to change from Acidophobe to Acidophile. The original E.Coli strand uses for this long-term evolution experiment, strand Bc251 had genetic traits such as T6r, Strr, R-, m-, Ara-, meaning that they couldn't grow on minimal medium that contained only Arabinose, due to their Ara operon being disabled). At the same time, Ara  mutations were introduced on half the population, due to genetic manipulation.

During the first half of the generational study, most of the colonies showed adapatability to grow using Glucose for their metabolism, which at the same time led to the appearances of defects in their DNA repair system that lead to millions of mutations in this time lapse. Although in normal conditions this would have been fatal for the strands, 10 or 20 mutations were found to be beneficial. 

One of the mutations, after several recombination cycles, lead to the appearance of a strand that could use Citrate as source of energy, instead of Glucose. Normally, Wild Type (WT) E.Coli can't transport citrate through the cell membrane to the cell interior, thus it cannot fixate citrate in the Citric Acid Cycle in the presence of Oxygen - Aerobic respiration). This has been one of the defining characteristics from E.Coli, thus the label of Acidophobe given to the bacteria. 

This lead to the final suggestion that there was a contingency  of two or more mutations that recombined in a non-adaptive potentiating mutation in the genes that lead to coding proteins that allowed for the transport of Citrate to the interior of E.Coli cells.  

This wasn't the only change observed in these strands. Normally, WT E.Coli have a cylindrical shape and these ones had a more round shape. This was due to changes in the coding of the PBP proteins (Peptidoglycan Binding Proteins) for the cellular wall of E.Coli. This proved to be an efficient mechanism to out-compete WT E.Coli in the conditions proposed in the long-term evolution experiments. Though this also had a downside, since these E.Coli strands had a larger sensitivity to osmotic stress, thus a lower survivability rate on stationary phase cultures (when the conditions of the experiment are no longer sustained).

Thus, the assumption that the defects of the DNA repair system was a downside to this experiment, this is largely incorrect. Indeed, had it not been for errors in the correction of mutations, these changes would have never taken part, as prior to every recombination and division cycle, bacterial cells go through a lot of cellular check-points to test for unwanted mutations, when the DNA repair system is working accordingly (normal rate of permitted errors in the DNA polymerase II is 10^-6).



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