Below is the abstract of an article in the latest edition of PLOS Biology. The scientists developed a method by which they could compare ‘evolved’ strains from the pure strains with which they’re been crossed. Under duress–that is, deprived of a glucose environment, and forced to live on galactose–they found that when four different strains of yeast were distressed in this way, all four strains developed the SAME type of adaptation in the SAME gene (GAL80), a gene which, in normal environments, suppresses the ‘galactose utilization pathway’.
Think about it: ALL four ‘evolved’ strains basically hit on the same mechanism. We certainly have change (mutation), but is it ‘random’ if each of the four strains reacts in the same way? How probable is it for a mutation to occur in the same place in all four strains while causing the same changed metabolic pathway to be set in motion? Random mutation? I think not.
High-Resolution Mutation Mapping Reveals Parallel Experimental Evolution in Yeast
Ayellet V. SegrÃƒÂ¨1, Andrew W. Murray1, Jun-Yi Leu1*Ã‚Â¤
1 Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, United States of America
Understanding the genetic basis of evolutionary adaptation is limited by our ability to efficiently identify the genomic locations of adaptive mutations. Here we describe a method that can quickly and precisely map the genetic basis of naturally and experimentally evolved complex traits using linkage analysis. A yeast strain that expresses the evolved trait is crossed to a distinct strain background and DNA from a large pool of progeny that express the trait of interest is hybridized to oligonucleotide microarrays that detect thousands of polymorphisms between the two strains. Adaptive mutations are detected by linkage to the polymorphisms from the evolved parent. We successfully tested our method by mapping five known genes to a precision of 0.2Ã¢â‚¬â€œ24 kb (0.1Ã¢â‚¬â€œ10 cM), and developed computer simulations to test the effect of different factors on mapping precision. We then applied this method to four yeast strains that had independently adapted to a fluctuating glucoseÃ¢â‚¬â€œgalactose environment. All four strains had acquired one or more missense mutations in GAL80, the repressor of the galactose utilization pathway. When transferred into the ancestral strain, the gal80 mutations conferred the fitness advantage that the evolved strains show in the transition from glucose to galactose. Our results show an example of parallel adaptation caused by mutations in the same gene.
Here’s the html link:
I haven’t read the entire article as yet, but I will shortly. I look forward to your reactions and thoughts.
Just one final note: isn’t it wondeful how evolution is so supple that it can explain all things. All you have to do is INVENT WORDS!!!
Here we have “parallel” adaptation (why not call it non-random, or directed mutation? That’s what is happening after all.), and then there’s “exaptation” (which really means that some anatomical structure that has a normal usage in some class of animals is now being employed for a completely different function in a related species with no known way of explaining how it came about because there is a lack of intermediate forms, and thus, ‘selective pressures’ to invoke. It’s really no more than another way of saying, “We don’t know how this change came about”. It just sounds better) and then, my favorite, “co-adaptation” (which is something that normally functions in one part, or organ, of an organism, and which is now found functioning in another part/organ of the animal that is performing a completely different function within the organism. This, again, is a word that is invented to get around having to explain how it is that one kind of gene is producing two kinds of effects. But simply inventing a word really doesn’t add to our understanding, does it?). Isn’t evolution great?