内复制
拟南芥
生物
泛素
细胞生物学
突变体
泛素连接酶
拟南芥
表型
遗传学
细胞周期
细胞
基因
作者
Xiaopeng Guo,Xin Zhang,Shan Jiang,Xin Qiao,Bolun Meng,X. J. Wang,Yanan Wang,Kaihuan Yang,Yilan Zhang,Na Li,Tianyan Chen,Yiyang Kang,Mengyi Yao,Xuan Zhang,Xinru Wang,Erling Zhang,Junhua Li,Dawei Yan,Zhubing Hu,José Ramón Botella
出处
期刊:Plant Physiology
[Oxford University Press]
日期:2023-10-18
卷期号:194 (2): 684-697
被引量:15
标识
DOI:10.1093/plphys/kiad559
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI