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指关节蛋白通过控制生长素分布和细胞分裂素活性来调节花分生组织的终止。

KNUCKLES regulates floral meristem termination by controlling auxin distribution and cytokinin activity.

作者信息

Wang Guangling, Wu Zhiyue, Sun Bo

机构信息

State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210023, China.

出版信息

Plant Cell. 2024 Dec 23;37(1). doi: 10.1093/plcell/koae312.

Abstract

The termination of floral meristem (FM) activity is essential for the normal development of reproductive floral organs. During this process, KNUCKLES (KNU), a C2H2-type zinc finger protein, crucially regulates FM termination by directly repressing the expression of both the stem cell identity gene WUSCHEL (WUS) and the stem cell marker gene CLAVATA3 (CLV3) to abolish the WUS-CLV3 feedback loop required for FM maintenance. In addition, phytohormones auxin and cytokinin are involved in FM regulation. However, whether KNU modulates auxin and cytokinin activities for FM determinacy control remains unclear. Here, we show that the auxin distribution and the cytokinin activity mediated by KNU in Arabidopsis (Arabidopsis thaliana) promote the termination of FM during stage 6 of flower development. Mutation of KNU leads to altered distribution of auxin and cytokinin in the FM of a stage 6 floral bud. Moreover, KNU directly represses the auxin transporter gene PIN-FORMED1 (PIN1) and the cytokinin biosynthesis gene ISOPENTENYLTRANSFERASE7 (IPT7) via mediating H3K27me3 deposition on these 2 loci to regulate auxin and cytokinin activities. Our study presents a molecular regulatory network that elucidates how the transcriptional repressor KNU integrates and modulates the activities of auxin and cytokinin, thus securing the timed FM termination.

摘要

花分生组织(FM)活性的终止对于生殖花器官的正常发育至关重要。在此过程中,C2H2型锌指蛋白KNUCKLES(KNU)通过直接抑制干细胞身份基因WUSCHEL(WUS)和干细胞标记基因CLAVATA3(CLV3)的表达来关键调控FM的终止,从而消除FM维持所需的WUS-CLV3反馈环。此外,植物激素生长素和细胞分裂素也参与FM调控。然而,KNU是否调节生长素和细胞分裂素活性以控制FM的确定性仍不清楚。在此,我们表明拟南芥中由KNU介导的生长素分布和细胞分裂素活性在花发育的第6阶段促进FM的终止。KNU的突变导致第6阶段花芽FM中生长素和细胞分裂素分布改变。此外,KNU通过介导H3K27me3在这两个位点的沉积直接抑制生长素转运蛋白基因PIN-FORMED1(PIN1)和细胞分裂素生物合成基因ISOPENTENYLTRANSFERASE7(IPT7),从而调节生长素和细胞分裂素活性。我们的研究提出了一个分子调控网络,阐明了转录抑制因子KNU如何整合和调节生长素和细胞分裂素的活性,从而确保FM适时终止。

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