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Modulation of secretion in Drosophila by amino‐acid starvation
Author(s) -
Rabouille Catherine
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.463.2
Subject(s) - secretion , biogenesis , microbiology and biotechnology , amino acid , biology , cytoplasm , secretory protein , drosophila melanogaster , signal transduction , biochemistry , chemistry , gene
Secretion is mediated by the secretory pathway that have a basic functional organisation very similar in Drosophila as in mammalian cells. Here, I will discuss evidence showing that secretion is be modulated by physiological conditions. Using Drosophila S2 cells, we have shown that amino‐acid starvation stimulates a pathway that inhibits secretion. This pathway relies on the atypical MAP Kinase ERK7 that we found is stabilised by amino acid starvation, leading in turn to the modification of Sec16, a key protein required for the functional organisation of the ER exit sites that are critical for secretion. Once modified, Sec16 no longer associates to ER membrane, ER exit site biogenesis is inhibited, and so is secretion as a whole. Furthermore, this pathway is independent of the TOR complex 1. These results indicate that secretion inhibition under amino‐acid starvation is an active mechanism requiring ERK7, not only a passive response to the absence of growth factors. Furthermore, they show that in the absence of nutrient, cytoplasm growth is inhibited via TORC1 inhibition whereas plasma membrane growth via secretion is inhibited independently.