BOTRYOID POLLEN 1 regulates ROS-triggered PCD and pollen wall development by controlling UDP-sugar homeostasis in rice
文献类型: 外文期刊
第一作者: Chen, Huiqiong
作者: Chen, Huiqiong;Zhang, Shuqing;Li, Ruiqi;Peng, Guoqing;Chen, Weipan;Liu, Minglong;Zhu, Liya;Xiao, Yueping;Ni, Jinlong;Liu, Zhenlan;Zhuang, Chuxiong;Xie, Yongyao;Chu, Zhizhan;Zhou, Hai;Chen, Huiqiong;Rautengarten, Carsten;Heazlewood, Joshua L.;Song, Fengshun;Ni, Jinlong;Wu, Aimin
作者机构:
期刊名称:PLANT CELL ( 影响因子:11.6; 五年影响因子:12.9 )
ISSN: 1040-4651
年卷期: 2023 年
页码:
收录情况: SCI
摘要: Uridine diphosphate (UDP)-sugars are important metabolites involved in the biosynthesis of polysaccharides and may be important signaling molecules. UDP-glucose 4-epimerase (UGE) catalyzes the interconversion between UDP-Glc and UDP-Gal, whose biological function in rice (Oryza sativa) fertility is poorly understood. Here, we identify and characterize the botryoid pollen 1 (bp1) mutant and show that BP1 encodes a UGE that regulates UDP-sugar homeostasis, thereby controlling the development of rice anthers. The loss of BP1 function led to massive accumulation of UDP-Glc and imbalance of other UDP-sugars. We determined that the higher levels of UDP-Glc and its derivatives in bp1 may induce the expression of NADPH oxidase genes, resulting in a premature accumulation of reactive oxygen species (ROS), thereby advancing programmed cell death (PCD) of anther walls but delaying the end of tapetal degradation. The accumulation of UDP-Glc as metabolites resulted in an abnormal degradation of callose, producing an adhesive microspore. Furthermore, the UDP-sugar metabolism pathway is not only involved in the formation of intine but also in the formation of the initial framework for extine. Our results reveal how UDP-sugars regulate anther development and provide new clues for cellular ROS accumulation and PCD triggered by UDP-Glc as a signaling molecule. UDP-Glc and its derivatives induce the expression of NADPH oxidase genes, inducing ROS-triggered PCD as signaling molecules, but also regulate pollen wall development as metabolites.
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