CLE42 delays leaf senescence by antagonizing ethylene pathway in Arabidopsis

© 2022 The Authors. New Phytologist © 2022 New Phytologist Foundation.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 235(2022), 2 vom: 20. Juli, Seite 550-562
1. Verfasser: Zhang, Yi (VerfasserIn)
Weitere Verfasser: Tan, Shuya, Gao, Yuhan, Kan, Chengcheng, Wang, Hou-Ling, Yang, Qi, Xia, Xinli, Ishida, Takashi, Sawa, Shinichiro, Guo, Hongwei, Li, Zhonghai
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2022
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Arabidopsis thaliana CLE EBF EIN3 ethylene leaf senescence Arabidopsis Proteins Ethylenes Plant Growth Regulators
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500 |a CommentIn: Trends Plant Sci. 2022 Oct;27(10):961-963. - PMID 35843831 
500 |a Citation Status MEDLINE 
520 |a © 2022 The Authors. New Phytologist © 2022 New Phytologist Foundation. 
520 |a Leaf senescence is the final stage of leaf development and is influenced by numerous internal and environmental factors. CLE family peptides are plant-specific peptide hormones that regulate various developmental processes. However, the role of CLE in regulating Arabidopsis leaf senescence remains unclear. Here, we found that CLE42 is a negative regulator of leaf senescence by using a CRISPR/Cas9-produced CLE mutant collection. The cle42 mutant displayed earlier senescence phenotypes, while overexpression of CLE42 delayed age-dependent and dark-induced leaf senescence. Moreover, application of the synthesized 12-amino-acid peptide (CLE42p) also delayed leaf senescence under natural and dark conditions. CLE42 and CLE41/44 displayed functional redundancy in leaf senescence, and the cle41 cle42 cle44 triple mutant displayed more pronounced earlier senescence phenotypes than any single mutant. Analysis of differentially expressed genes obtained by RNA-Seq methodology revealed that the ethylene pathway was suppressed by overexpressing CLE42. Moreover, CLE42 suppressed ethylene biosynthesis and thus promoted the protein accumulation of EBF, which in turn decreased the function of EIN3. Accordingly, mutation of EIN3/EIL1 or overexpression of EBF1 suppressed the earlier senescence phenotypes of the cle42 mutant. Together, our results reveal that the CLE peptide hormone regulates leaf senescence by communicating with the ethylene pathway 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Arabidopsis thaliana 
650 4 |a CLE 
650 4 |a EBF 
650 4 |a EIN3 
650 4 |a ethylene 
650 4 |a leaf senescence 
650 7 |a Arabidopsis Proteins  |2 NLM 
650 7 |a Ethylenes  |2 NLM 
650 7 |a Plant Growth Regulators  |2 NLM 
700 1 |a Tan, Shuya  |e verfasserin  |4 aut 
700 1 |a Gao, Yuhan  |e verfasserin  |4 aut 
700 1 |a Kan, Chengcheng  |e verfasserin  |4 aut 
700 1 |a Wang, Hou-Ling  |e verfasserin  |4 aut 
700 1 |a Yang, Qi  |e verfasserin  |4 aut 
700 1 |a Xia, Xinli  |e verfasserin  |4 aut 
700 1 |a Ishida, Takashi  |e verfasserin  |4 aut 
700 1 |a Sawa, Shinichiro  |e verfasserin  |4 aut 
700 1 |a Guo, Hongwei  |e verfasserin  |4 aut 
700 1 |a Li, Zhonghai  |e verfasserin  |4 aut 
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