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Wat, L. W.

Publications and source records attributed to Wat, L. W..

2 recordsLinked to original sources

A low sugar diet enhances Drosophila body size in males and females via sex-specific mechanisms

In Drosophila, changes to dietary protein elicit different body size responses between the sexes. Whether this sex difference in nutrient-dependent body size regulation extends to other nutrients, such as dietary sugar, remains unclear. Here, we show that reducing dietary sugar enhanced body size in Drosophila male and female larvae. Indeed, the largest body size was found in larvae reared in a diet without added sugar. Despite the equivalent body size effects of a low sugar diet between males and females, we detected sex-specific changes to the insulin/insulin-like growth factor (IIS) and target of rapamycin (TOR) signaling pathways. Further, we show that the metabolic changes observed in larvae reared on a low sugar diet differ between the sexes. Thus, despite identical phenotypic responses to dietary sugar in males and females, distinct changes to cell signaling pathways and whole-body metabolism were associated with the increased body size in each sex. This highlights the importance of including both sexes in all mechanistic studies on larval growth, as males and females may use different molecular and metabolic mechanisms to achieve similar phenotypic outcomes.

physiology

Female-specific upregulation of insulin pathway activity mediates the sex difference in Drosophila body size plasticity

Nutrient-dependent body size plasticity differs between the sexes in most species, including mammals. Previous work in Drosophila showed that body size plasticity was higher in females, yet the mechanisms underlying the sex difference in body size plasticity remain unclear. Here, we discover that a protein-rich diet augments body size in females and not males because of a female-specific increase in activity of the conserved insulin/insulin-like growth factor signaling pathway (IIS). This increased IIS activity was triggered by a diet-induced increase in stunted, and required Drosophila insulin-like peptide 2, illuminating new sex-specific roles for these genes. Importantly, we show that sex determination gene transformer regulates the diet-induced increase in stunted and IIS activity, and mediates the sex difference in body size plasticity. This identifies one sex-specific mechanism underlying the nutrient-dependent regulation of IIS activity and body size plasticity, providing vital insight into conserved mechanisms that mediate sex differences in phenotypic plasticity.

physiology