Physiological starvation increases EGF-Ras-MAPK pathway activity during C. elegans vulval induction

摘要: Studying how molecular pathways respond to ecologically relevant environmental variation is fundamental understand organismal development and its evolution. Here we characterize starvation modulates Caenorhabditis elegans vulval cell fate patterning – an environmentally sensitive process, with a nevertheless robust output. Past research has shown many mutants affecting EGF-Ras-MAPK, Delta-Notch Wnt be suppressed by factors, such as starvation. aimed resolve previous, seemingly contradictory, observations on levels of induction. Using the strong suppression Vulvaless phenotype lin-3/egf reduction-of-function mutations experimental paradigm, first tested for possible involvement sensory system in relaying signals affect induction: mutation various inputs, DAF-2/Insulin or DAF-7/TGF-b signaling did not abolish lin-3(rf) suppression. In contrast, nutrient deprivation induced intestinal peptide transporter gene pept-1 TOR pathway component rsks-1 (the orthologue mammalian P70S6K) very strongly mutant phenotypes. Therefore, physiologically starved animals these tightly recapitulated effects external While both RNAi were sufficient increase Ras Notch activities cells, highly penetrant tissue-specific null allele lin-3 was either condition. This additional results indicate that partial expression required These suggest cross-talk between deprivation, TOR-S6K EGF-Ras-MAPK during C.