Rice RuBisCO activase promotes the dark-induced leaf senescence by enhancing the degradation of filamentation temperature-sensitive H
文献类型: 外文期刊
作者: Zhang, Yanli 1 ; Dong, Guojun 2 ; Wu, Xiaoyue 1 ; Chen, Fei 1 ; Ruan, Banpu 1 ; Jiang, Yaohuang 1 ; Zhang, Ying 1 ; Liu, Lu 3 ; Yuan, Yao-Wu 4 ; Wu, Limin 1 ; Wei, Jian 3 ; Qian, Qian 2 ; Yu, Yanchun 1 ;
作者机构: 1.Hangzhou Normal Univ, Coll Life & Environm Sci, Hangzhou 310036, Peoples R China
2.China Natl Rice Res Inst, State Key Lab Rice Biol, Hangzhou 310006, Zhejiang, Peoples R China
3.Jilin Agr Univ, Fac Agron, Changchun 130000, Peoples R China
4.Univ Connecticut, Dept Ecol & Evolutionary Biol, Storrs, CT 06269 USA
关键词:
rice (
期刊名称:PLANT JOURNAL ( 影响因子:5.7; 五年影响因子:7.0 )
ISSN: 0960-7412
年卷期: 2025 年 121 卷 4 期
页码:
收录情况: SCI
摘要: Leaf senescence is a complex process that is triggered by many developmental and environmental factors. However, the mechanisms regulating leaf senescence remain unclear. Here, we revealed that rice ribulose-1,5-bisphosphate carboxylase/oxygenase activase (RCA) promotes the onset of basal dark-induced senescence. RCA was mainly expressed in the leaves, and its expression level quickly declined under dark conditions. Furthermore, rca mutant plants presented a prolonged leaf longevity phenotype in the dark, whereas overexpression of the large isoform of RCA (RCAL), not small isoform (RCAS), in rice and Arabidopsis accelerated leaf senescence. Filamentation temperature-sensitive H (OsFtsH1), a zinc metalloprotease, interacts with RCAL and RCAS and presents a higher binding efficiency to RCAL than RCAS in darkness. Furthermore, we found that RCAL promotes 26S proteasome-mediated degradation of OsFtsH1 protein, which can be inhibited by protease inhibitor MG132. Consequently, OsFtsH1 loss-of-function mutants exhibit accelerated leaf senescence, whereas OsFtsH1-overexpressing plants display delayed senescence. Collectively, our findings highlight the significant role of RCAL isoform in regulating leaf senescence under dark conditions, particularly through enhancing the degradation of OsFtsH1.
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