Posted: Dec 23, 2010 3:11 pm
As I read it, Behe was careful to distinguish between the molecular function and the phenotypic function. The phenotype might have a function, but Behe was restricting his paper to only molecular function, which might not seem to apply at the level of a whole limb (as there may be a number of molecular functions affecting a limb). I don't know a whole lot about genetics in detail so the following illustration may not be a good one, but in terms of what Behe was discussing, if a mutation occurred that prevented an inhibitor from activating due to a point mutation, preventing restriction of size of a limb part for example then Behe would consider that a loss of function mutation, even if the change in size allowed a new morphological function, e.g. allowing a fin to be used for propulsion along the bottom, or to be impressive to attract a mate, as well as a previous function of steering while swimming.
However, at the molecular level would it be easier to identify a loss of function, since a function is already known, than to determine gain of function, where a function for the new form would need to be determined? Could this influence the ratio of loss to gain observed in the studies? In a similar way deleterious mutations in humans may be better known because they are relevant to medicine and appear as medical problems, whereas beneficial mutations may be harder to identify.
However, at the molecular level would it be easier to identify a loss of function, since a function is already known, than to determine gain of function, where a function for the new form would need to be determined? Could this influence the ratio of loss to gain observed in the studies? In a similar way deleterious mutations in humans may be better known because they are relevant to medicine and appear as medical problems, whereas beneficial mutations may be harder to identify.