Fig 1.
HLH-30/TFEB regulates a complex transcriptional network critical for nutrient sensing and starvation defenses.
In wild-type C. elegans under starvation conditions, HLH-30 activates lysosome biogenesis and catabolic pathways, which encourage starvation survival and prime the animal for recovery from starvation upon re-feeding. Without HLH-30, C. elegans fail to induce lipolytic and lysosomal genes such as lipl-2 and VHA genes, leading to diminished starvation survival and failure to recover from starvation once food is reintroduced. Murphy and colleagues in this edition of PLOS Biology report that simple nutrients glucose and linoleic acid can bypass the need for HLH-30 in recovery from starvation. It remains unknown how glucose and linoleic acid bypass the need for HLH-30 but at least in part it may be through restoration of lysosomal function and mTORC1 activity downstream of HLH-30 action. HLH-30, helix-loop-helix family member 30; mTORC1, mechanistic target of rapamycin complex 1; TFEB, transcription factor EB; VHA, vacuolar H+-ATPase.