E3 ligases MAC3A and MAC3B ubiquitinate UBIQUITIN-SPECIFIC PROTEASE14 to regulate organ size in Arabidopsis.
E3 ligases MAC3A and MAC3B ubiquitinate UBIQUITIN-SPECIFIC PROTEASE14 to regulate organ size in Arabidopsis.
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E3连接酶MAC3A和MAC3B泛素化泛素特异性蛋白酶14调节拟南芥器官大小。
DOI：
10.1093/plphys/kiad559
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发表时间：
2024-01-31
期刊：
影响因子：
7.4
通讯作者：
Guo, Siyi
中科院分区：
文献类型：
--
作者：
Guo, Xiaopeng;Zhang, Xin;Jiang, Shan;Qiao, Xin;Meng, Bolun;Wang, Xiaohang;Wang, Yanan;Yang, Kaihuan;Zhang, Yilan;Li, Na;Chen, Tianyan;Kang, Yiyang;Yao, Mengyi;Zhang, Xuan;Wang, Xinru;Zhang, Erling;Li, Junhua;Yan, Dawei;Hu, Zhubing;Botella, Jose Ramon;Song, Chun-Peng;Li, Yunhai;Guo, Siyi
在植物发育过程中控制器官大小的分子机制最终影响作物产量。然而，对这些机制仍然缺乏深入的了解。泛素特异性蛋白酶14（UBP 14）是由DA 3编码的决定拟南芥器官大小的重要因子。在此，我们鉴定了da 3 -1突变体表型的两个抑制子，即da 3 - 11和2的抑制子（SUD 1和SUD 2），其分别编码E3连接酶M0 S4相关复合物3A（MAC 3A）和MAC 3B。mac 3a-1和mac 3b-1突变部分抑制了da 3 -1突变体中观察到的高倍性水平和器官大小表型。生化分析表明，MAC 3A和MAC 3B与UBP 14/DA 3物理相互作用并泛素化以调节其稳定性。我们以前报道过UBP 14/DA 3作用于B型细胞周期蛋白依赖性激酶CDKB 1;1的上游，并保持其稳定性以抑制细胞内复制和细胞生长。在这项工作中，发现MAC 3A和MAC 3B通过泛素化UBP 14/DA 3促进CDKB 1;1的降解。遗传分析表明，MAC 3A和MAC 3B与UBP 14/DA 3在共同的通路中起作用，以控制核内复制和器官大小。因此，我们的研究结果定义了一个调控模块，MAC 3A/MAC 3B-UBP 14-CDKB 1;1，在决定拟南芥器官大小和核内复制中起着关键作用。2个抑制子的分析揭示了E3连接酶MAC 3A和MAC 3B影响泛素特异性蛋白酶14的稳定性以控制植物器官大小的分子和遗传机制。
The molecular mechanisms controlling organ size during plant development ultimately influence crop yield. However, a deep understanding of these mechanisms is still lacking. UBIQUITIN-SPECIFIC PROTEASE14 (UBP14), encoded by DA3, is an essential factor determining organ size in Arabidopsis (Arabidopsis thaliana). Here, we identified two suppressors of the da3-1 mutant phenotype, namely SUPPRESSOR OF da3-1 1 and 2 (SUD1 and SUD2), which encode the E3 ligases MOS4-ASSOCIATED COMPLEX 3A (MAC3A) and MAC3B, respectively. The mac3a-1 and mac3b-1 mutations partially suppressed the high ploidy level and organ size phenotypes observed in the da3-1 mutant. Biochemical analysis showed that MAC3A and MAC3B physically interacted with and ubiquitinated UBP14/DA3 to modulate its stability. We previously reported that UBP14/DA3 acts upstream of the B-type cyclin-dependent kinase CDKB1;1 and maintains its stability to inhibit endoreduplication and cell growth. In this work, MAC3A and MAC3B were found to promote the degradation of CDKB1;1 by ubiquitinating UBP14/DA3. Genetic analysis suggests that MAC3A and MAC3B act in a common pathway with UBP14/DA3 to control endoreduplication and organ size. Thus, our findings define a regulatory module, MAC3A/MAC3B-UBP14-CDKB1;1, that plays a critical role in determining organ size and endoreduplication in Arabidopsis. Analysis of 2 suppressors uncovers the molecular and genetic mechanisms by which E3 ligases MAC3A and MAC3B affect the stability of UBIQUITIN-SPECIFIC PROTEASE14 to control plant organ size.
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影响因子：
7.2
作者：
Doelling, JH;Yan, N;Vierstra, RD
通讯作者：
Vierstra, RD
影响因子：
7.4
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作者：
Clough, SJ;Bent, AF
通讯作者：
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