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Regulation of subtelomeric silencing during stress response.

Identifieur interne : 001970 ( Main/Exploration ); précédent : 001969; suivant : 001971

Regulation of subtelomeric silencing during stress response.

Auteurs : Wandong Ai [États-Unis] ; Paula G. Bertram ; Chi Kwan Tsang ; Ting Fung Chan ; X F Steven Zheng

Source :

RBID : pubmed:12504006

Descripteurs français

English descriptors

Abstract

Sir proteins play a critical role in silent chromatin domains. While mutations can cause derepression of heterochromatin, it remains unclear whether silencing is actively involved in transcriptional control under changing environmental conditions. We find that TOR inhibits Sir3 phosphorylation. Rapamycin or stress induced by chlorpromazine leads to activation of MAP kinase Mpk1/Slt2, which phosphorylates Sir3. Sir3 hyperphosphorylation is correlated with reduced subtelomeric silencing, increased subtelomeric cell wall gene expression, and stress resistance to chlorpromazine, but does not affect the silent HML and rDNA loci. Based on these observations, we propose that regulation of silencing may be used to control gene expression at specific silent chromatin domains in response to stress and possibly other environmental changes.

DOI: 10.1016/s1097-2765(02)00695-0
PubMed: 12504006


Affiliations:


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Le document en format XML

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<term>Mitogen-Activated Protein Kinases (metabolism)</term>
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<div type="abstract" xml:lang="en">Sir proteins play a critical role in silent chromatin domains. While mutations can cause derepression of heterochromatin, it remains unclear whether silencing is actively involved in transcriptional control under changing environmental conditions. We find that TOR inhibits Sir3 phosphorylation. Rapamycin or stress induced by chlorpromazine leads to activation of MAP kinase Mpk1/Slt2, which phosphorylates Sir3. Sir3 hyperphosphorylation is correlated with reduced subtelomeric silencing, increased subtelomeric cell wall gene expression, and stress resistance to chlorpromazine, but does not affect the silent HML and rDNA loci. Based on these observations, we propose that regulation of silencing may be used to control gene expression at specific silent chromatin domains in response to stress and possibly other environmental changes.</div>
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