Using RNA-seq to understand the endocrine control of condition-dependent traits


Meeting Abstract

15-5  Monday, Jan. 4 11:00  Using RNA-seq to understand the endocrine control of condition-dependent traits. ZINNA, R.*; EMLEN, D.; LAVINE, L.C.; DWORKIN, I.; Washington State University; University of Montana; Washington State University; McMaster University robert.zinna@wsu.edu

Across animal species, competition for females has encouraged ever more extreme morphologies. In many cases the condition dependent growth of these structures is mediated by endocrine signals. The insulin signaling pathway has been shown to specifically mediate this growth in horned rhinoceros beetles. In addition, the critical insect hormone juvenile hormone (JH) has been shown play a role in condition dependent growth in this species. Upregulation of JH during horn growth has no measurable effect on horn size, contrary to the effect of this hormone in other beetles. On the other hand, downregulation through RNAi knockdown of the JH receptor Methoprene-tolerant (Met) decreased relative horn size. Here we test the hypothesis that partial co-option of downstream members of the JH pathway mediates condition dependent growth of rhinoceros beetle weapons. RNA-seq analysis of developing horn tissue from beetles raised in different nutritional conditions provides support for this hypothesis. Key JH pathway members (such as Met) are indeed upregulated in horns from high-condition males. However, members farther downstream (such as Broad) do not show differential expression patterns. In comparison, virtually all members of the insulin-signaling pathway show upregulation in high-condition males. This correlates with functional data- RNAi knockdown of the insulin receptor decreases relative horn size to a much larger degree than knockdown of the JH receptor, and accordingly fewer pathway members are upregulated during horn growth in the latter pathway. Our data show that the evolution of endocrine regulation of traits, and the relative importance of their signals, can drive the evolution of even similar structures.

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