Host cell factor-1 recruitment to E2F-bound and cell-cycle-control genes is mediated by THAP11 and ZNF143.
Host cell factor-1 recruitment to E2F-bound and cell-cycle-control genes is mediated by THAP11 and ZNF143.
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DOI：
10.1016/j.celrep.2014.09.051
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发表时间：
2014-11-06
期刊：
影响因子：
8.8
通讯作者：
Chakravarti D
中科院分区：
文献类型：
--
作者：
Parker JB;Yin H;Vinckevicius A;Chakravarti D
宿主细胞因子-1（HCF-1）是后生动物细胞周期进程和细胞增殖所必需的转录辅助调节因子。目前的模型表明，HCF-1作为E2 F蛋白的直接共调节因子发挥作用，促进细胞增殖所需基因的表达。在这份报告中，我们表明，HCF-1招聘到许多E2 F结合的启动子是由锌指转录因子THAP 11和ZNF 143的协同作用介导的，而不是E2 F蛋白直接。THAP 11、ZNF 143和HCF-1在染色质上形成相互依赖的复合物，该复合物与E2 F占用无关。THAP 11/ZNF 143/HCF-1复合物的破坏导致细胞周期控制基因的表达改变，并导致细胞增殖、细胞周期进展和细胞活力降低。这些数据建立了一个新的模型，表明THAP 11/ZNF 143/HCF-1复合物是控制细胞增殖的转录调控网络的关键组成部分。
Host cell factor-1 (HCF-1) is a metazoan transcriptional co-regulator essential for cell cycle progression and cell proliferation. Current models suggest a mechanism whereby HCF-1 functions as a direct co-regulator of E2F proteins, facilitating the expression of genes necessary for cell proliferation. In this report, we show that HCF-1 recruitment to numerous E2F-bound promoters is mediated by the concerted action of zinc finger transcription factors THAP11 and ZNF143, rather than E2F proteins directly. THAP11, ZNF143, and HCF-1 form a mutually dependent complex on chromatin, which is independent of E2F occupancy. Disruption of the THAP11/ZNF143/HCF-1 complex results in altered expression of cell cycle control genes and leads to reduced cell proliferation, cell cycle progression, and cell viability. These data establish a new model which suggests that a THAP11/ZNF143/HCF-1 complex is a critical component of the transcriptional regulatory network governing cell proliferation.
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