期刊
PLANTS-BASEL
卷 10, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/plants10112418
关键词
Arabidopsis; chromosome segregation; DMC1; female meiosis; K11-linked; megaspore mother cell; ubiquitin-conjugating enzyme; UBC22
资金
- Natural Sciences and Engineering Research Council of Canada [RGPIN-2018-05834]
- Science and Technology Program of Fujian Province [2019N5008, 31970333]
- China Postdoctoral Science Foundation
UBC22 is critical for normal chromosome segregation in female meiosis but not for male meiosis, and DMC1 distribution is abnormal in mutant female meiocytes, leading to frequent aneuploids among the mutant plants due to abnormal DNA content in female mutant gametes. These results provide important leads for studying the role of UBC22 and K11-linked ubiquitination.
Protein ubiquitination is important for the regulation of meiosis in eukaryotes, including plants. However, little is known about the involvement of E2 ubiquitin-conjugating enzymes in plant meiosis. Arabidopsis UBC22 is a unique E2 enzyme, able to catalyze the formation of ubiquitin dimers through lysine 11 (K11). Previous work has shown that ubc22 mutants are defective in megasporogenesis, with most ovules having no or abnormally functioning megaspores; furthermore, some mutant plants show distinct phenotypes in vegetative growth. In this study, we showed that chromosome segregation and callose deposition were abnormal in mutant female meiosis while male meiosis was not affected. The meiotic recombinase DMC1, required for homologous chromosome recombination, showed a dispersed distribution in mutant female meiocytes compared to the presence of strong foci in WT female meiocytes. Based on an analysis of F1 plants produced from crosses using a mutant as the female parent, about 24% of female mutant gametes had an abnormal content of DNA, resulting in frequent aneuploids among the mutant plants. These results show that UBC22 is critical for normal chromosome segregation in female meiosis but not for male meiosis, and they provide important leads for studying the role of UBC22 and K11-linked ubiquitination.
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