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ATX1 生成的 H3K4me3 对于 ATX1 调控基因的转录延伸(而非起始)是必需的。

ATX1-generated H3K4me3 is required for efficient elongation of transcription, not initiation, at ATX1-regulated genes.

机构信息

School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China.

出版信息

PLoS Genet. 2012;8(12):e1003111. doi: 10.1371/journal.pgen.1003111. Epub 2012 Dec 20.

DOI:10.1371/journal.pgen.1003111
PMID:23284292
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3527332/
Abstract

Tri-methylated H3 lysine 4 (H3K4me3) is associated with transcriptionally active genes, but its function in the transcription process is still unclear. Point mutations in the catalytic domain of ATX1 (ARABIDOPSIS TRITHORAX1), a H3K4 methyltransferase, and RNAi knockdowns of subunits of the AtCOMPASS-like (Arabidopsis Complex Proteins Associated with Set) were used to address this question. We demonstrate that both ATX1 and AtCOMPASS-like are required for high level accumulation of TBP (TATA-binding protein) and Pol II at promoters and that this requirement is independent of the catalytic histone modifying activity. However, the catalytic function is critically required for transcription as H3K4me3 levels determine the efficiency of transcription elongation. The roles of H3K4me3, ATX1, and AtCOMPASS-like may be of a general relevance for transcription of Trithorax-activated eukaryotic genes.

摘要

三甲基化 H3 赖氨酸 4(H3K4me3)与转录活跃的基因有关,但它在转录过程中的功能尚不清楚。通过点突变 ATX1(拟南芥 TRITHORAX1)的催化结构域,一种 H3K4 甲基转移酶,以及 AtCOMPASS-like(拟南芥复合物蛋白与 SET 相关)亚基的 RNAi 敲低,解决了这个问题。我们证明 ATX1 和 AtCOMPASS-like 都需要 TBP(TATA 结合蛋白)和 Pol II 在启动子处的高水平积累,并且这种需求独立于催化组蛋白修饰活性。然而,催化功能对于转录至关重要,因为 H3K4me3 水平决定了转录延伸的效率。H3K4me3、ATX1 和 AtCOMPASS-like 的作用可能对转录激活的真核基因具有普遍意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/35bd236a5be7/pgen.1003111.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/482e3b038b3c/pgen.1003111.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/e7fde43b119e/pgen.1003111.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/75ed15835d3a/pgen.1003111.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/35bd236a5be7/pgen.1003111.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/482e3b038b3c/pgen.1003111.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/9cefdec190bd/pgen.1003111.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/2166c88695a0/pgen.1003111.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/18bece500418/pgen.1003111.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/751496b577cf/pgen.1003111.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/e7fde43b119e/pgen.1003111.g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2cd3/3527332/35bd236a5be7/pgen.1003111.g008.jpg

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