Distinct Molecular Mechanisms Regulate Feeding State-Dependent CO2 Chemotaxis Plasticity During Different Life Stages in Caenorhabditis elegans.
TL;DR
It is identified that animals employ distinct molecular mechanisms to achieve equivalent modulation of CO2-chemosensory behaviour at different developmental stages, and neural circuits at different life stages may utilize distinct, stage-specific molecular mechanisms to induce identical plasticity in chemosensory behaviour.
Abstract
Across developmental stages, animals modulate their behavioural responses to external cues according to intrinsic physiological states. During development, particularly in juvenile stages, nervous systems undergo extensive changes at multiple levels. However, it remains unclear whether nervous systems at different developmental stages utilize the same underlying molecular mechanisms to produce equivalent behavioural modulations in response to intrinsic or extrinsic cues. Using the model organism Caenorhabditis elegans, we identify that animals employ distinct molecular mechanisms to achieve equivalent modulation of CO2-chemosensory behaviour at different developmental stages. Ubiquitin-proteasome-mediated downregulation of the insulin/IGF receptor, DAF-2, by the conserved quality-control ubiquitin ligase CHN-1/CHIP in the CO2-sensing BAG neurons promotes attraction to environmental CO2 during the starvation-induced L1-arrest stage. In contrast, CO2-attraction in dauer animals is independent of CHN-1/CHIP activity. Furthermore, the feeding-induced reversal of CO2-chemotaxis to avoidance during L1-arrest exit requires the insulin/IGF pathway and the conserved CRH-1/CREB1 transcription factor activity in the BAG neurons. However, the onset of CO2-avoidance during dauer exit is independent of CRH-1/CREB1 activity. These findings suggest that neural circuits at different life stages may utilize distinct, stage-specific molecular mechanisms to induce identical plasticity in chemosensory behaviour.