Global proteomic- and transcriptomic analyses of starvation responses reveal a central role for lipoprotein metabolism in acute starvation survival in C. elegans

The molecular mechanisms underlying the physiological and cellular response to starvation are still not fully understood. We have used quantitative proteomics and RNA-seq to examine the temporal responses to starvation in the multicellular organism C. elegans, comparing the response in both wild type animals and in animals lacking the transcription factor HLH-30. Our findings show that starvation alters the abundance of hundreds of proteins and mRNAs in a temporal manner, many of which are involved in central metabolic pathways including lipoprotein metabolism. We show that hlh-30 animals die prematurely when starved, which can be prevented by knockdown of either vit-1 or vit-5, encoding two different lipoproteins. We show that the size and number of intestinal lipid droplets under starvation are altered in hlh-30 animals, that can be rescued by knockdown of vit-1, indicating that rescue of survival of hlh-30 animals under starvation conditions is closely linked to the size and number of intestinal lipid droplets. hh-30 mutants and wild type Caenorhabditis elegans