The MAPKKKs Ste11 and Bck1 jointly transduce the high oxidative stress signal through the cell wall integrity MAP kinase pathway

Microbial Cell

卷:2

Chunyan Jin¹  Stephen K. Kim²  Katrina F. Cooper²  Stephen D. Willis² 

[1] Current address: Shaoxing Women and Children Hospital, 305 East Street, Shaoxing, Zhejiang, China, 312000.;

[2] Department of Molecular Biology, Rowan University School of Osteopathic Medicine, Stratford, NJ, 08055 USA.;

关键词: cyclin C;    oxidative stress;    protein degradation;    programmed cell death;    MAPK signal transduction pathways;    mitochondrial morphology;   

DOI  :  10.15698/mic2015.09.226

来源: DOAJ

【 摘 要 】

Oxidative stress stimulates the Rho1 GTPase, which in turn induces the cell wall integrity (CWI) MAP kinase cascade. CWI activation promotes stress-responsive gene expression through activation of transcription factors (Rlm1, SBF) and nuclear release and subsequent destruction of the repressor cyclin C. This study reports that, in response to high hydrogen peroxide exposure, or in the presence of constitutively active Rho1, cyclin C still translocates tothecytoplasmandisdegradedincellslackingBck1,theMAPKKKofthe CWIpathway.However,inmutantsdefectiveforboth Bck1andSte11,the MAPKKKfromthehighosmolarity,pseudohyphalandmatingMAPKpathways,cyclinCnucleartocytoplasmicrelocalizationanddestructionisprevented.FurtheranalysisrevealedthatcyclinCgoesfromadiffusenuclear signal to a terminal nucleolar localization in this double mutant. Live cell imaging confirmed that cyclin C transiently passes through the nucleolus prior to cytoplasmicentryinwild-typecells.Takentogetherwithpreviousstudies, these results indicate that under low levels of oxidative stress, Bck1 activation is sufficient to induce cyclin C translocation and degradation. However, higher stressconditionsalsostimulateSte11,whichreinforcesthestresssignalto cyclin C and other transcription factors. This model would provide a mechanismbywhichdifferentstresslevelscanbesensed andinterpretedbythe cell.

【 授权许可】

Unknown