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TRXG 蛋白 ULT1 通过与 TCP14/15 相互作用来调节拟南芥器官大小,拮抗 LIM 肽酶 DA1 对靶基因上 H3K4me3 的作用。

The trxG protein ULT1 regulates Arabidopsis organ size by interacting with TCP14/15 to antagonize the LIM peptidase DA1 for H3K4me3 on target genes.

机构信息

Biotechnology Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China.

State Key Laboratory of Crop Gene Resources and Breeding, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing 100081, China.

出版信息

Plant Commun. 2024 Apr 8;5(4):100819. doi: 10.1016/j.xplc.2024.100819. Epub 2024 Jan 12.

DOI:10.1016/j.xplc.2024.100819
PMID:38217289
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11009162/
Abstract

Plant organ size is an important agronomic trait that makes a significant contribution to plant yield. Despite its central importance, the genetic and molecular mechanisms underlying organ size control remain to be fully clarified. Here, we report that the trithorax group protein ULTRAPETALA1 (ULT1) interacts with the TEOSINTE BRANCHED1/CYCLOIDEA/PCF14/15 (TCP14/15) transcription factors by antagonizing the LIN-11, ISL-1, and MEC-3 (LIM) peptidase DA1, thereby regulating organ size in Arabidopsis. Loss of ULT1 function significantly increases rosette leaf, petal, silique, and seed size, whereas overexpression of ULT1 results in reduced organ size. ULT1 associates with TCP14 and TCP15 to co-regulate cell size by affecting cellular endoreduplication. Transcriptome analysis revealed that ULT1 and TCP14/15 regulate common target genes involved in endoreduplication and leaf development. ULT1 can be recruited by TCP14/15 to promote lysine 4 of histone H3 trimethylation at target genes, activating their expression to determine final cell size. Furthermore, we found that ULT1 influences the interaction of DA1 and TCP14/15 and antagonizes the effect of DA1 on TCP14/15 degradation. Collectively, our findings reveal a novel epigenetic mechanism underlying the regulation of organ size in Arabidopsis.

摘要

植物器官大小是一个重要的农艺性状,对植物产量有重要贡献。尽管其具有核心重要性,但器官大小控制的遗传和分子机制仍有待充分阐明。在这里,我们报告称,三结构域蛋白 ULTRAPETALA1(ULT1)通过拮抗 LIN-11、ISL-1 和 MEC-3(LIM)肽酶 DA1 与 TEOSINTE BRANCHED1/CYCLOIDEA/PCF14/15(TCP14/15)转录因子相互作用,从而调节拟南芥的器官大小。ULT1 功能丧失会显著增加头状花序叶、花瓣、蒴果和种子的大小,而过表达 ULT1 则会导致器官大小减小。ULT1 与 TCP14 和 TCP15 结合,通过影响细胞内有丝分裂来共同调节细胞大小。转录组分析显示,ULT1 和 TCP14/15 通过调节参与有丝分裂和叶片发育的共同靶基因来调节细胞大小。ULT1 可以被 TCP14/15 招募,以促进靶基因组蛋白 H3 赖氨酸 4 的三甲基化,激活其表达,从而决定最终的细胞大小。此外,我们发现 ULT1 影响 DA1 和 TCP14/15 的相互作用,并拮抗 DA1 对 TCP14/15 降解的影响。总之,我们的研究结果揭示了拟南芥器官大小调控的一种新的表观遗传机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/3386de31fb7f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/d411dc3c0b2c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/7af142af99c3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/7b2006b979be/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/40ddc6bc1dbd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/4d2b4a0fc0e4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/4843ef241eb1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/3386de31fb7f/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/d411dc3c0b2c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/7af142af99c3/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/7b2006b979be/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/40ddc6bc1dbd/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/4d2b4a0fc0e4/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/4843ef241eb1/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5176/11009162/3386de31fb7f/gr7.jpg

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