interdigital webbing, however, is due to the specific inhibition of at least three BMP activities in the post-outgrowth phase of the interdigital regions (Weatherbee et al., 2006).).
The finch and bat examples involve the control of differential growth and differential apoptosis (in the case of the interdigital webbing in bats) at key phases by regulation of expression of members of the TGF-β family, specifically of the BMP subfamily of this superfamily. In contrast, the loss of stickleback pelvic armature in at least three independent speciation events involves the transcriptional down-regulation of a specific key TF, namely Pitx1. The genetic analysis indicates that this loss of armature, which appears to be adaptive as an energy-saving measure in lakes that are essentially predator-free zones, also involves several minor loci (as determined by quantitative trait locus analysis), but the key major locus is Pitx1, and the loss of pelvic regional expression of this TF is due, apparently, to mutations in cis-linked enhancer modules that normally boost its specific regional activity (Shapiro et al., 2004).).
As informative and important as the findings of these impressive studies are, they provide only the first stage of an understanding of the respective cases. This is most obvious in the differential growth stories of finch beaks and bat wings. In these cases, the pinpointed key molecules whose changes in amount are essential for the developmental process are well known components of ubiquitously used signal transduction pathways. Those pathways are used in a host of different developmental processes, with a wide range of different phenotypic outcomes, both within and amongst the different animal systems in which they are used. Such ubiquitously used regulatory modules have been termed “plug-ins” by Eric Davidson (2006). It follows that identifying neither the particular plug-in module nor, even less, a particular rate-limiting component (e.g., BMP2, calmodulin, BMP4) can fully explain the developmental change that lies at the heart of the respective evolutionary change. The still missing parts of the explanation, in all of these instances, involve the genetic network of which the respective identified molecule is a part and how that network then regulates selective cell proliferation (and apoptosis in the case of the bat’s interdigital webbing) in the relevant developing primordium.
At first glance, however, the loss of pelvic armature in sticklebacks seems to present quite a different situation. Ignoring, for the moment, the relatively small contributions from the minor loci that contribute to the phenotype, the key element in explaining the phenotypic change is a change in expression in one gene, namely the TF gene Pitx1. One does not need to understand in detail what genes Pitx1 regulates, in specifying the development of the pelvic armature, to understand how down-regulation of its expression in selected sites leads to the loss of that structure, with