» Articles » PMID: 31165143

The Insulin Signaling Substrate Chico and the Ecdysone Response Element Broad Both Regulate Growth of the Head Horns in the Asian Rhinoceros Beetle, Trypoxylus Dichotomus

Overview
Specialty Biology
Date 2019 Jun 6
PMID 31165143
Citations 2
Authors
Affiliations
Soon will be listed here.
Abstract

Males of the Asian rhinoceros beetle, Trypoxylus dichotomus, possess exaggerated head and thoracic horns that scale dramatically out of proportion to body size. While RNAi-mediated knockdowns of the insulin receptor suggest that the insulin signaling pathway regulates nutrition-dependent growth including exaggerated horns, the genes that regulate disproportionate growth have yet to be identified. We used RNAi-mediated knockdown of several genes to investigate their potential role in growth and scaling of the sexually dimorphic, exaggerated head horns of T. dichotomus. Knockdown of the insulin signaling substrate chico and the ecdysone response element broad caused significant decreases in head horn length, while having no or minimal effects on other structures such as elytra and tibiae. However, scaling of horns to body size was not affected by either knockdown. In addition, knockdown of phosphatase and tensin homolog, a negative regulator of the insulin signaling pathway, had no significant effects on any trait. Our results do not identify any candidate genes that may specifically mediate the allometric aspect of horn growth, but they do confirm the insulin signaling pathway as a mediator of conditional trait expression, and importantly implicate the ecdysone signaling pathway, possibly in conjunction with insulin signaling, as an additional mediator of horn growth.

Citing Articles

The Genetic Basis Underpinning Sexually Selected Traits across Different Animal Lineages: Are There Genetic Mechanisms in Common?.

Kang J Animals (Basel). 2024; 14(6).

PMID: 38539938 PMC: 10967623. DOI: 10.3390/ani14060841.


Evolution of sexual development and sexual dimorphism in insects.

Hopkins B, Kopp A Curr Opin Genet Dev. 2021; 69:129-139.

PMID: 33848958 PMC: 8364864. DOI: 10.1016/j.gde.2021.02.011.