Abstract
Starvation is among the most ancient of selection pressures, driving evolution of a robust arsenal of starvation survival defenses. In order to survive starvation stress, organisms must be able to curtail anabolic processes during starvation and judiciously activate catabolic pathways. Although the activation of metabolic defenses in response to nutrient deprivation is an obvious component of starvation survival, less appreciated is the importance of the ability to recover from starvation upon re-exposure to nutrients. In order for organisms to successfully recover from starvation, cells must be kept in a state of ready so that upon the return of nutrients, activities such as growth and reproduction can be resumed. Critical to this state of ready is the lysosome, an organelle that provides essential signals of nutrient sufficiency to cell growth-activating pathways in the fed state. In this issue, Murphy and colleagues provide evidence that exposure of Caenorhabditis elegans roundworms to 2 simple nutrients, glucose and the polyunsaturated fatty acid linoleate, is able to render lysosomal function competent to activate key downstream starvation recovery pathways, bypassing the need for a master transcriptional regulator of lysosomes. These findings provide a quantum leap forward in our understanding of the cellular determinants that permit organisms to survive cycles of feast and famine.
Highlights
It is rare for organisms to encounter constant food supply in the wild
A report in the current edition of PLOS Biology shows that the C. elegans ancestral gene for the MiT/transcription factor E (TFE) transcription factor family hlh-30 is required to couple lysosomal nutrient sensing to survival during nutrient stress, probably by providing critical metabolites required for recovery from breakdown of complex substrates in lysosomes [27]
Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis of transcriptomewide RNA sequencing (RNAseq) data demonstrate that starved hlh30 mutant worms displayed altered levels of gene transcripts encoding proteins involved in amino acid metabolism, fatty acid metabolism, and lysosomal function compared with their wild-type counterparts
Summary
It is rare for organisms to encounter constant food supply in the wild. More commonly, animals are exposed to extended periods where food is scarce and must execute metabolic defenses to survive the stress of nutrient deprivation. Previous studies have identified AMPK and mechanistic target of rapamycin complex 1 (mTORC1) as cellular, nutrient-sensing protein kinases that respond antagonistically to alterations in cellular energy and nutrient levels under starvation and feeding [9].
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