Genomic analysis of COP9 signalosome function in Drosophila melanogaster reveals a role in temporal regulation of gene expression.

Genomic analysis of COP9 signalosome function in Drosophila melanogaster reveals a role in temporal regulation of gene expression.
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果蝇中COP9信号体功能的基因组分析揭示了基因表达的时间调节中的作用。

DOI:
10.1038/msb4100150
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发表时间:
2007
影响因子:
9.9
通讯作者:
Chamovitz, Daniel A.
Chamovitz, Daniel A.
中科院分区:
生物学1区
文献类型:
--
作者:
Oron, Efrat;Tuller, Tamir;Li, Ling;Rozovsky, Nina;Yekutieli, Daniel;Rencus-Lazar, Sigal;Segal, Daniel;Chor, Benny;Edgar, Bruce A.;Chamovitz, Daniel A.

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COP9 信号体 (CSN) 是一种八亚基蛋白质复合物,在所有高等真核生物中都是保守的。 CSN 与泛素-蛋白酶体通路交叉,调节控制发育各个方面的信号通路。我们使用果蝇作为模型系统来阐明这一重要复合体的功能。生成了四个 csn 突变体的转录组数据,在三个发育时间点采样。我们的结果具有高度可重复性,并使用需要不同微阵列和不同对照的两种不同实验装置得到证实。我们的结果表明,CSN 在果蝇发育过程中充当转录抑制因子,导致 csn 突变体中基因表达的慢性化。对公开的果蝇转录组数据进行的“时移”分析表明,CSN 抑制的基因通常主要在胚胎发生晚期或变态过程中被诱导。这些时间变化可能是由于 CSN 在调节转录因子中的作用所致。 CSN 亚基 4 的无效突变和 csn5 的亚等位突变导致比 csn5 无效突变株中所见的缺陷更严重,表明 CSN5 仅携带部分 CSN 功能。
The COP9 signalosome (CSN), an eight-subunit protein complex, is conserved in all higher eukaryotes. CSN intersects the ubiquitin–proteasome pathway, modulating signaling pathways controlling various aspects of development. We are using Drosophila as a model system to elucidate the function of this important complex. Transcriptome data were generated for four csn mutants, sampled at three developmental time points. Our results are highly reproducible, being confirmed using two different experimental setups that entail different microarrays and different controls. Our results indicate that the CSN acts as a transcriptional repressor during development of Drosophila, resulting in achronic gene expression in the csn mutants. ‘Time shift' analysis with the publicly available Drosophila transcriptome data indicates that genes repressed by the CSN are normally induced primarily during late embryogenesis or during metamorphosis. These temporal shifts are likely due to the roles of the CSN in regulating transcription factors. A null mutation in CSN subunit 4 and hypomorphic mutations in csn5 lead to more severe defects than seen in the csn5-null mutants strain, suggesting that CSN5 carries only some of the CSN function.
DOI: 10.1534/genetics.106.058099
发表时间: 2006-09-01
期刊: GENETICS
影响因子: 3.3
作者:
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通讯作者: Mackay, Trudy F. C.
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期刊: PLANT CELL
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发表时间: 2005-07-01
期刊: PLANT CELL
影响因子: 11.6
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发表时间: 1996-03-01
期刊: PLANT PHYSIOLOGY
影响因子: 7.4
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DOI: 10.1016/s0960-9822(00)80023-8
发表时间: 1999-10-21
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者:
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通讯作者: Chamovitz, DA