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酵母细胞核内沉默区室的证据:端粒接近度和Sir蛋白浓度在沉默子介导的基因抑制中的作用。

Evidence for silencing compartments within the yeast nucleus: a role for telomere proximity and Sir protein concentration in silencer-mediated repression.

作者信息

Maillet L, Boscheron C, Gotta M, Marcand S, Gilson E, Gasser S M

机构信息

Laboratoire de Biologie Moléculaire et Cellulaire de l'Ecole Normale Supérieure de Lyon, France.

出版信息

Genes Dev. 1996 Jul 15;10(14):1796-811. doi: 10.1101/gad.10.14.1796.

DOI:10.1101/gad.10.14.1796
PMID:8698239
Abstract

Transcriptional repression at the silent mating-type loci in yeast requires the targeting of silent information regulator (Sir) proteins through specific interactions formed at cis-acting silencer elements. We show here that a reporter gene flanked by two functional silencers is not repressed when integrated at >200 kb from a telomere. Repression is restored by creation of a new telomere 13 kb from the integrated reporter or by elevated expression of SIR1, SIR3, and/or SIR4. Coupled expression represses in an additive manner, suggesting that all three factors are in limiting concentrations. When overexpressed, Sir3 and Sir4 are dispersed throughout the nucleoplasm, in contrast to wild-type cells where they are clustered in a limited number of foci together with telomeres. Efficient silencer function thus seems to require either proximity to a pool of concentrated Sir proteins, that is, proximity to telomeres, or delocalization of the silencing factors.

摘要

酵母中沉默交配型基因座处的转录抑制需要通过在顺式作用沉默元件处形成的特异性相互作用将沉默信息调节因子(Sir)蛋白靶向定位。我们在此表明,当一个两侧带有两个功能性沉默子的报告基因整合在距离端粒>200 kb处时,它不会被抑制。通过在距离整合的报告基因13 kb处创建一个新的端粒,或者通过提高SIR1、SIR3和/或SIR4的表达,可以恢复抑制作用。协同表达以累加的方式起抑制作用,这表明所有这三个因子都处于有限的浓度。当Sir3和Sir4过表达时,它们会分散在整个核质中,这与野生型细胞不同,在野生型细胞中它们与端粒一起聚集在有限数量的位点上。因此,有效的沉默子功能似乎需要要么靠近浓缩的Sir蛋白池,即靠近端粒,要么使沉默因子去定位。

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Evidence for silencing compartments within the yeast nucleus: a role for telomere proximity and Sir protein concentration in silencer-mediated repression.酵母细胞核内沉默区室的证据:端粒接近度和Sir蛋白浓度在沉默子介导的基因抑制中的作用。
Genes Dev. 1996 Jul 15;10(14):1796-811. doi: 10.1101/gad.10.14.1796.
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