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自主途径复合物的特征,促进拟南芥开花。

Characterization of an autonomous pathway complex that promotes flowering in Arabidopsis.

机构信息

National Institute of Biological Sciences, Beijing 102206, China.

PTN Joint Graduate Program, School of Life Sciences, Tsinghua University, Beijing 100084, China.

出版信息

Nucleic Acids Res. 2022 Jul 22;50(13):7380-7395. doi: 10.1093/nar/gkac551.

DOI:10.1093/nar/gkac551
PMID:35766439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9303297/
Abstract

Although previous studies have identified several autonomous pathway components that are required for the promotion of flowering, little is known about how these components cooperate. Here, we identified an autonomous pathway complex (AuPC) containing both known components (FLD, LD and SDG26) and previously unknown components (EFL2, EFL4 and APRF1). Loss-of-function mutations of all of these components result in increased FLC expression and delayed flowering. The delayed-flowering phenotype is independent of photoperiod and can be overcome by vernalization, confirming that the complex specifically functions in the autonomous pathway. Chromatin immunoprecipitation combined with sequencing indicated that, in the AuPC mutants, the histone modifications (H3Ac, H3K4me3 and H3K36me3) associated with transcriptional activation are increased, and the histone modification (H3K27me3) associated with transcriptional repression is reduced, suggesting that the AuPC suppresses FLC expression at least partially by regulating these histone modifications. Moreover, we found that the AuPC component SDG26 associates with FLC chromatin via a previously uncharacterized DNA-binding domain and regulates FLC expression and flowering time independently of its histone methyltransferase activity. Together, these results provide a framework for understanding the molecular mechanism by which the autonomous pathway regulates flowering time.

摘要

虽然先前的研究已经确定了几个自主途径的组成部分,这些组成部分对于促进开花是必需的,但对于这些组成部分如何合作知之甚少。在这里,我们鉴定了一个自主途径复合物(AuPC),它包含已知的组成部分(FLD、LD 和 SDG26)和以前未知的组成部分(EFL2、EFL4 和 APRF1)。所有这些成分的功能丧失突变都会导致 FLC 表达增加和开花延迟。延迟开花的表型与光周期无关,可以通过春化作用克服,这证实了该复合物特异性地在自主途径中发挥作用。染色质免疫沉淀结合测序表明,在 AuPC 突变体中,与转录激活相关的组蛋白修饰(H3Ac、H3K4me3 和 H3K36me3)增加,而与转录抑制相关的组蛋白修饰(H3K27me3)减少,这表明 AuPC 通过调节这些组蛋白修饰至少部分抑制 FLC 的表达。此外,我们发现 AuPC 成分 SDG26 通过以前未表征的 DNA 结合结构域与 FLC 染色质结合,并独立于其组蛋白甲基转移酶活性调节 FLC 表达和开花时间。总之,这些结果为理解自主途径调节开花时间的分子机制提供了一个框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/6fc45fef4a64/gkac551fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/3870c606c56f/gkac551fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/204197c0ed95/gkac551fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/17f89d355d73/gkac551fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/8a8ab090aea4/gkac551fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/1c16193d9b03/gkac551fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/6fc45fef4a64/gkac551fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/3870c606c56f/gkac551fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/204197c0ed95/gkac551fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/17f89d355d73/gkac551fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/8a8ab090aea4/gkac551fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/1c16193d9b03/gkac551fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f460/9303297/6fc45fef4a64/gkac551fig6.jpg

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