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HCC1, a Polygalacturonase, Regulates Chlorophyll Degradation via the Ethylene Synthesis Pathway

Chlorophyll degradation is an important physiological process and is essential for plant growth and development. However, how chlorophyll degradation is controlled at the cellular and molecular level remains largely elusive. Pectin is a main component of the primary cell wall, and polygalacturonases...

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Published in:Rice 2023-12, Vol.16 (1), p.57-57, Article 57
Main Authors: Liao, Yongxiang, Xiang, Bing, Xue, Zhenzhen, Ali, Asif, Li, Yong, Li, Mengyuan, Wei, Aiji, Xin, Jialu, Guo, Daiming, Liao, Yingxiu, Tian, Yunfeng, Zhao, Zhixue, Xu, Peizhou, Zhang, Hongyu, Chen, Xiaoqiong, Liu, Yutong, Zhou, Hao, Xia, Duo, Du, Kangxi, Wu, Xianjun
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Language:English
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Summary:Chlorophyll degradation is an important physiological process and is essential for plant growth and development. However, how chlorophyll degradation is controlled at the cellular and molecular level remains largely elusive. Pectin is a main component of the primary cell wall, and polygalacturonases (PGs) is a group of pectin-hydrolases that cleaves the pectin backbone and release oligogalacturonide. Whether and how PGs affect chlorophyll degradation metabolism and its association with ethylene (ETH) have not been reported before. Here, we report a novel function of PG in a mutant ‘ high chlorophyll content1’ hcc1 , which displayed a decrease in growth and yield. Our morphological, biochemical and genetic analyses of hcc1 , knockout lines and complementation lines confirm the function of HCC1 in chlorophyll degradation. In hcc1 , the PG activity, ETH content and D-galacturonic acid (D-GA) was significantly decreased and showed an increase in the thickness of the cell wall. Exogenous application of ETH and D-GA can increase ETH content and induce the expression of HCC1 , which further can successfully induce the chlorophyll degradation in hcc1 . Together, our data demonstrated a novel function of HCC1 in chlorophyll degradation via the ETH pathway.
ISSN:1939-8425
1939-8433
1934-8037
DOI:10.1186/s12284-023-00675-8