机构地区:[1]Institute of Biochemistry, Zhejiang University, Hangzhou 310058, China [2]State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
出 处:《Acta Biochimica et Biophysica Sinica》2009年第7期594-602,共9页生物化学与生物物理学报(英文版)
基 金:Acknowledgements We thank Dr Stillman D.J. for providing S. cerevisiae plasmid BD1. Funding This work was supported by the grants from the National Science Foundation of China (30700006 and 30600008) and China Postdoctoral Science Foundation (20070421197).
摘 要:Here we reported that, in Saccharomyces cerevisiae, deleting Swil (ScSwil), a core component in Swi/Snf complex, caused defects of invasive growth, pseudohyphal growth, FLOll expression, and proper cell separation. Re-introduction of SWII into the swil mutants could suppress all defects observed. We also showed that overproducing Swil could suppress the defect offlo8 cells in pseudohyphal growth in diploids, but not invasive growth in haploids. Overexpression of SWII could not bypass the requirement of Ste12 or Tecl in invasive growth or pseudohyphal growth. We concluded that the Swi/Snf complex was required for FLO11 expression and proper cell separation, and both the FL08 and STE12 genes should be present for the complex to function for the invasive growth but only the STE12 gene was required for the pseudohyphal growth. Ectopic expression of Candida albicans SWI1 (CaSWII) could partially complement the defects examined of haploid Scswil mutants, but failed to complement the defects examined of diploid Scswil/ Scswil mutants. Overexpressing CaSwil mitigated invasive and pseudohyphal growth defects resulting from deletions in the MAP kinase and cAMP pathways. The integrity of S. cerevisiae Swi/Snf complex is required for invasive and filamentous growth promoted by overexpressing CaSwil.Here we reported that, in Saccharomyces cerevisiae, deleting Swil (ScSwil), a core component in Swi/Snf complex, caused defects of invasive growth, pseudohyphal growth, FLOll expression, and proper cell separation. Re-introduction of SWII into the swil mutants could suppress all defects observed. We also showed that overproducing Swil could suppress the defect offlo8 cells in pseudohyphal growth in diploids, but not invasive growth in haploids. Overexpression of SWII could not bypass the requirement of Ste12 or Tecl in invasive growth or pseudohyphal growth. We concluded that the Swi/Snf complex was required for FLO11 expression and proper cell separation, and both the FL08 and STE12 genes should be present for the complex to function for the invasive growth but only the STE12 gene was required for the pseudohyphal growth. Ectopic expression of Candida albicans SWI1 (CaSWII) could partially complement the defects examined of haploid Scswil mutants, but failed to complement the defects examined of diploid Scswil/ Scswil mutants. Overexpressing CaSwil mitigated invasive and pseudohyphal growth defects resulting from deletions in the MAP kinase and cAMP pathways. The integrity of S. cerevisiae Swi/Snf complex is required for invasive and filamentous growth promoted by overexpressing CaSwil.
关 键 词:ScSwil CaSwil invasive growth pseudohyphal growth FLO11 SACCHAROMYCESCEREVISIAE
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