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Control of entry into meiosis and quiescence in budding yeast
Author(s) -
Sarkar Sourav,
Millar Jonathan,
Arumugam Prakash
Publication year - 2013
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.27.1_supplement.1031.13
Subject(s) - meiosis , meiosis ii , biology , protein phosphatase 2 , microbiology and biotechnology , signal transduction , phosphatase , kinase , serine , yeast , caenorhabditis elegans , phosphorylation , maturation promoting factor , genetics , cell cycle , cyclin , cell , gene
How cells sense changes in environment and mount a response is a fundamental question in biology. Nutrition starvation in budding yeast has been an useful model to study this biological trait. When yeast cells are deprived of essential nutrients they can either enter a quiescent state (referred to as G 0 ) or enter meiosis to form spores that can stay dormant for long periods of time. Precisely how environmental signals are sensed by yeast cells to trigger quiescence/meiosis is not known. Signals from multiple nutrient‐sensing signal transduction pathways converge on a serine‐threonine kinase called Rim15 which integrates the signals to orchestrate entry into quiescence or gametogenesis. In this we have identified a signalling pathway (REP) consisting of a serine‐threonine kinase Rim15, c‐AMP protein Igo1 and protein phosphatase PP2A Cdc55 which regulates entry into both quiescence and meiosis. PP2A Cdc55 negatively regulates entry into meiosis and G 0 . On nutrient starvation, Rim15 becomes active and phosphorylates endosulfines at Serine‐64 to convert it into an inhibitor of PP2A Cdc55 thereby promoting entry into meiosis and G 0 . Remarkably a similar pathway controls entry into mitosis in mammalian cells.