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基因特异性转录抑制与全染色体转录抑制之间的分子联系。

A molecular link between gene-specific and chromosome-wide transcriptional repression.

作者信息

Chu Diana S, Dawes Heather E, Lieb Jason D, Chan Raymond C, Kuo Annie F, Meyer Barbara J

机构信息

Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720-3204, USA.

出版信息

Genes Dev. 2002 Apr 1;16(7):796-805. doi: 10.1101/gad.972702.

Abstract

Gene-specific and chromosome-wide mechanisms of transcriptional regulation control development in multicellular organisms. SDC-2, the determinant of hermaphrodite fate in Caenorhabditis elegans, is a paradigm for both modes of regulation. SDC-2 represses transcription of X chromosomes to achieve dosage compensation, and it also represses the male sex-determination gene her-1 to elicit hermaphrodite differentiation. We show here that SDC-2 recruits the entire dosage compensation complex to her-1, directing this X-chromosome repression machinery to silence an individual, autosomal gene. Functional dissection of her-1 in vivo revealed DNA recognition elements required for SDC-2 binding, recruitment of the dosage compensation complex, and transcriptional repression. Elements within her-1 differed in location, sequence, and strength of repression, implying that the dosage compensation complex may regulate transcription along the X chromosome using diverse recognition elements that play distinct roles in repression.

摘要

基因特异性和全染色体范围的转录调控机制控制着多细胞生物体的发育。SDC-2是秀丽隐杆线虫雌雄同体命运的决定因素,是这两种调控模式的一个范例。SDC-2抑制X染色体的转录以实现剂量补偿,它还抑制雄性性别决定基因her-1以引发雌雄同体分化。我们在此表明,SDC-2将整个剂量补偿复合体招募到her-1,引导这种X染色体抑制机制沉默一个单独的常染色体基因。对her-1在体内的功能剖析揭示了SDC-2结合、剂量补偿复合体的招募和转录抑制所需的DNA识别元件。her-1内的元件在位置、序列和抑制强度上有所不同,这意味着剂量补偿复合体可能利用在抑制中发挥不同作用的多种识别元件沿着X染色体调控转录。

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本文引用的文献

1
Common themes in mechanisms of gene silencing.基因沉默机制中的常见主题。
Mol Cell. 2001 Sep;8(3):489-98. doi: 10.1016/s1097-2765(01)00340-9.
5
Chromosome cohesion, condensation, and separation.染色体黏连、凝聚和分离。
Annu Rev Biochem. 2000;69:115-44. doi: 10.1146/annurev.biochem.69.1.115.

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