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The phospholipase B homolog, Plb1, and the cAMP•protein kinase A pathway function cooperatively to regulate an osmotic stress‐induced growth control system in fission yeast
Author(s) -
Matsuo Yasuhiro,
McInnis Brittney,
Marcus Stevan
Publication year - 2008
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.22.1_supplement.639.2
Subject(s) - protein kinase a , schizosaccharomyces pombe , microbiology and biotechnology , biology , osmotic shock , mutant , camp dependent pathway , signal transduction , biochemistry , kinase , gene
The phospholipase B homolog, Plb1p, and the cAMP•protein kinase A (PKA) pathway are essential for growth of the fission yeast, Schizosaccharomyces pombe , under high salinity conditions. While plb1Δ , adenylate cyclase ( cyr1Δ ), and PKA ( pka1Δ ) mutants are not hypersensitive to sorbitol, we show here that plb1Δ cyr1Δ and plb1Δ pka1Δ double mutants are hypersensitive to both sorbitol and low salt concentrations whereas cyr1Δ pka1Δ mutants are phenotypically similar to the respective single mutants, thus demonstrating that Plb1p and the cAMP•PKA pathway function cooperatively in mediating hypertonic stress response in S. pombe. Hypertonic stress‐induced growth arrest is both asynchronous and reversible in the plb1Δ pka1Δ double mutant as well as the respective single mutants, indicating that Plb1p and the cAMP•PKA pathway are required for cell cycle progression in hypertonic media but not for survival of hypertonic stress. Deletion of cgs1 , which encodes a Pka1p regulatory subunit, partially rescues the hypertonic stress‐induced growth defect of plb1Δ cyr1Δ cells, providing further evidence of functional interaction between Plb1 and the cAMP•PKA pathway. Pka1‐GFP fusion proteins are localized in the cytoplasm and concentrated in the nucleus, the latter in a cAMP‐dependent, Cgs1p‐independent fashion, under normal growth conditions and exported from the nucleus in response to prolonged hypertonic stress.