Meeting Abstract

77.4  Monday, Jan. 6 09:00  Identification of two novel insulin- and hormone-regulated nutritional checkpoints in C. elegans development SCHINDLER, AJ*; BAUGH, LR; SHERWOOD, DR; Duke University adam.schindler@duke.edu

Developing organisms in the wild exist in complex environments in which the availability of food varies. When faced with nutritional scarcity, organisms slow or arrest development and undergo physiological adaptations. It is not well understood how organisms sense nutritional scarcity and systemically modify development. To address these questions, we examined the C. elegans starvation response during larval development and identify two previously uncharacterized nutritionally regulated checkpoints in the L3 and L4 larval stages. Tissue development arrests at precise times in each larval stage, remains arrested for several days, and resumes upon re-feeding. Two conserved pathways that mediate the L3 and L4 response to starvation are insulin-like signaling and steroid hormone signaling. A FoxO transcription factor, DAF-16, becomes nuclear-localized in response to reduced insulin signaling and is required for the timely response to nutrient withdrawal. It functions at least partly to inhibit steroid hormone secretion that systemically promotes developmental progression. In the absence of daf-16 or when steroid hormones are overexpressed, animals continue development during starvation, leading to aberrant morphologies and shortened survival. These results demonstrate that C. elegans arrest development at precise times in response to starvation and highlight the genetic pathways that link nutritional status with developmental progression. The key pathways of nutritional response are conserved and may reflect an ancestral means of rapidly modifying growth and development in response to changing environmental conditions.