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[Spanky]

Originally posted by cheval de frise
SHP, soup and balt already laid out the theory. The protocol requires an understanding of which specific mutations have which (cumulative) effects, often at different points in a biochemical and developmental cascade. One has to correlate phenotypic effects with specific genetic changes, understand what direct effect (if any) those changes have on gene expression (i.e., level/developmental timing/duration), regulatory feedback loops, resultant protein sequences and conformational consequences (protein folding is a four-dimensional process)...and so on. These are complex questions but they do have answers. Geneticists and biochemists are working on all of these problems now. As other posters have said, the probability that a SINGLE mutation could be responsible for the development of an entire organ is zero. Scientists are sequencing and deciphering non-human genomes as we type. The mouse genome was published recently, as was (I believe) the chimpanzee genome. Comparative genetics has already provided significant insights. We have a plan for getting the information that will answer your specific question, and are going about obtaining that information...unlike proponents of certain alternative "theories."

By the way, evolution is a fact, not a theory, at least at the micro level. Scientists have directly observed and altered the characteristics of lab bacteria by manipulating their environments over thousands of successive generations. One can selectively "evolve" bacteria that tolerate certain poisons or do not need certain nutrients. Natural processes have also resulted in such organisms. Blind cavefish with vestigial eyes are on the path towards ridding themselves of those organs. Once a transposon-driven (or direct) mutation inactivates the gene(s) responsible for ocular structural development -- and that mutation doesn't result in negative selective pressure because their environment doesn't require eyes -- eyeless cavefish will appear in increased numbers proportional to the overall population (known in human genetics as "the founder effect"). It's a messy process. There is evidence that certain attributes have evolved more than once, then died out as other, more beneficial mutations confer additional advantages in populations not having the original mutation. Environment plays a gigantic role. There are multiple false starts. At the end of the day, though, it is fairly clear how the overall process works. The biochemical details simply take a lot of parallel work (and computer power) to figure out.

Ramen.

CDF (on the one day I happen to visit the board for old times' sake, y'all have a GENETICS discussion???? I'm having flashbacks to MY prior professional life.)

(Edited to fix formatting)

Game. Set. Match.