Singh Harpreet, Erkine Alexander M, Kremer Selena B, Duttweiler Harry M, Davis Donnie A, Iqbal Jabed, Gross Rachel R, Gross David S
Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932, USA.
Genetics. 2006 Apr;172(4):2169-84. doi: 10.1534/genetics.105.052738. Epub 2006 Feb 1.
We report the results of a genetic screen designed to identify transcriptional coregulators of yeast heat-shock factor (HSF). This sequence-specific activator is required to stimulate both basal and induced transcription; however, the identity of factors that collaborate with HSF in governing noninduced heat-shock gene expression is unknown. In an effort to identify these factors, we isolated spontaneous extragenic suppressors of hsp82-deltaHSE1, an allele of HSP82 that bears a 32-bp deletion of its high-affinity HSF-binding site, yet retains its two low-affinity HSF sites. Nearly 200 suppressors of the null phenotype of hsp82-deltaHSE1 were isolated and characterized, and they sorted into six expression without heat-shock element (EWE) complementation groups. Strikingly, all six groups contain alleles of genes that encode subunits of Mediator. Three of the six subunits, Med7, Med10/Nut2, and Med21/Srb7, map to Mediator's middle domain; two subunits, Med14/Rgr1 and Med16/Sin4, to its tail domain; and one subunit, Med19/Rox3, to its head domain. Mutations in genes encoding these factors enhance not only the basal transcription of hsp82-deltaHSE1, but also that of wild-type heat-shock genes. In contrast to their effect on basal transcription, the more severe ewe mutations strongly reduce activated transcription, drastically diminishing the dynamic range of heat-shock gene expression. Notably, targeted deletion of other Mediator subunits, including the negative regulators Cdk8/Srb10, Med5/Nut1, and Med15/Gal11 fail to derepress hsp82-deltaHSE1. Taken together, our data suggest that the Ewe subunits constitute a distinct functional module within Mediator that modulates both basal and induced heat-shock gene transcription.
我们报告了一项旨在鉴定酵母热休克因子(HSF)转录共调节因子的遗传筛选结果。这种序列特异性激活剂对于刺激基础转录和诱导转录均是必需的;然而,在调控未诱导的热休克基因表达过程中与HSF协同作用的因子的身份尚不清楚。为了鉴定这些因子,我们分离了hsp82 - deltaHSE1的自发基因外抑制子,hsp82 - deltaHSE1是HSP82的一个等位基因,其高亲和力HSF结合位点有一个32 bp的缺失,但仍保留其两个低亲和力HSF位点。我们分离并鉴定了近200个hsp82 - deltaHSE1无效表型的抑制子,它们被分为六个无热休克元件(EWE)互补组。引人注目的是,所有六个组都包含编码中介体亚基的基因的等位基因。六个亚基中的三个,即Med7、Med10 / Nut2和Med21 / Srb7,定位于中介体的中间结构域;两个亚基,Med14 / Rgr1和Med16 / Sin4,定位于其尾部结构域;一个亚基,Med19 / Rox3,定位于其头部结构域。编码这些因子的基因突变不仅增强了hsp82 - deltaHSE1的基础转录,也增强了野生型热休克基因的基础转录。与它们对基础转录的影响相反,更严重的ewE突变强烈降低激活转录,极大地减少了热休克基因表达的动态范围。值得注意的是,靶向缺失其他中介体亚基,包括负调节因子Cdk8 / Srb10、Med5 / Nut1和Med15 / Gal11,未能解除对hsp82 - deltaHSE1的抑制。综上所述,我们的数据表明,EWE亚基在中介体内构成一个独特的功能模块,可调节基础和诱导的热休克基因转录。