Figure 4.

Proposed model for the regulation of horn and genitalia allometries by insulin signalling and interacting pathways. (a) Regulation of high levels of nutritional responsiveness during horn formation across a nutritional gradient. Low nutrition conditions result in the upregulation of Foxo, promoting smoothened (smo) expression in the process (directly or indirectly), which in turn inhibits proliferation of horn tissue, resulting in a hornless male phenotype (this study and [22]). In these individuals, Foxo^RNAi results in the disinhibition and induction of horn growth. In intermediate-sized males, Foxo acts as a growth sensitizer resulting in disproportionate growth responses and the reduction in horn growth in Foxo^RNAi individuals. Lastly, high nutrition conditions result in Foxo-independent expression of the male isoform of doublesex (dsxm) and the promotion of horn proliferation [21]. Results presented here provide partial support that InR2 expression promotes dsxm expression under these conditions (thus InR2 is presented in parentheses). (b) Regulation of low levels of nutritional responsiveness during genitalia growth across a nutritional gradient. Foxo inhibits genitalia growth under low nutrition condition, but promotes genitalia growth under high nutrition conditions. As a consequence, Foxo^RNAi males possess relative larger genitalia under low nutrition condition, but relatively smaller under high nutrition conditions, resulting in a shallower genitalia–body size allometry. By contrast, InR1 and InR2 promote genitalia growth regardless of nutritional conditions (figure 2), and InR1/2^RNAi results in reduced genitalia sizes across the entire range of body sizes. How InR1/2 and Foxo interact during genitalia formation remains to be determined. Effect size is indicated by font size, and blue arrows and orange bars indicate interactions (growth induction or inhibition, respectively) supported by RNAi or qRT-PCR data (this study and [21,22]). (Online version in colour.)