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L型细胞周期蛋白CYL-1和热休克因子HSF-1是秀丽隐杆线虫热休克诱导蛋白表达所必需的。

The L-type cyclin CYL-1 and the heat-shock-factor HSF-1 are required for heat-shock-induced protein expression in Caenorhabditis elegans.

作者信息

Hajdu-Cronin Yvonne M, Chen Wen J, Sternberg Paul W

机构信息

Howard Hughes Medical Institute and Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.

出版信息

Genetics. 2004 Dec;168(4):1937-49. doi: 10.1534/genetics.104.028423.

DOI:10.1534/genetics.104.028423
PMID:15611166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1448743/
Abstract

In a screen for suppressors of activated GOA-1 (Galpha(o)) under the control of the hsp-16.2 heat-shock promoter, we identified three genetic loci that affected heat-shock-induced GOA-1 expression. The cyl-1 mutants are essentially wild type in appearance, while hsf-1 and sup-45 mutants have egg-laying defects. The hsf-1 mutation also causes a temperature-sensitive developmental arrest, and hsf-1 mutants have decreased life span. Western analysis indicated that mutations in all three loci suppressed the activated GOA-1 transgene by decreasing its expression. Heat-shock-induced expression of hsp-16.2 mRNA was reduced in cyl-1 mutants and virtually eliminated in hsf-1 and sup-45 mutants, as compared to wild-type expression. The mutations could also suppress other transgenes under heat-shock control. cyl-1 and sup-45, but not hsf-1, mutations suppressed a defect caused by a transgene not under heat-shock control, suggesting a role in general transcription or a post-transcriptional aspect of gene expression. hsf-1 encodes the C. elegans homolog of the human heat-shock factor HSF1, and cyl-1 encodes a cyclin most similar to cyclin L. We believe HSF-1 acts in heat-shock-inducible transcription and CYL-1 acts more generally in gene expression.

摘要

在一项针对受hsp - 16.2热休克启动子控制的活化GOA - 1(Gαo)抑制子的筛选中,我们鉴定出三个影响热休克诱导的GOA - 1表达的基因位点。cyl - 1突变体在外观上基本为野生型,而hsf - 1和sup - 45突变体存在产卵缺陷。hsf - 1突变还导致温度敏感的发育停滞,且hsf - 1突变体寿命缩短。蛋白质免疫印迹分析表明,这三个位点的突变均通过降低其表达来抑制活化的GOA - 1转基因。与野生型表达相比,热休克诱导的hsp - 16.2 mRNA在cyl - 1突变体中减少,在hsf - 1和sup - 45突变体中几乎消除。这些突变也能抑制热休克控制下的其他转基因。cyl - 1和sup - 45突变(而非hsf - 1突变)抑制了一个不受热休克控制的转基因导致的缺陷,这表明其在一般转录或基因表达的转录后方面发挥作用。hsf - 1编码人热休克因子HSF1的秀丽隐杆线虫同源物,cyl - 1编码一种与细胞周期蛋白L最相似的细胞周期蛋白。我们认为HSF - 1在热休克诱导的转录中起作用,而CYL - 1在基因表达中发挥更广泛的作用。

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