Arabidopsis UBC13 differentially regulates two programmed cell death pathways in responses to pathogen and low-temperature stress

Bibliographische Detailangaben
Veröffentlicht in:	The New phytologist. - 1979. - 221(2019), 2 vom: 12. Jan., Seite 919-934
1. Verfasser:	Wang, Lipu (VerfasserIn)
Weitere Verfasser:	Wen, Rui, Wang, Jinghe, Xiang, Daoquan, Wang, Qian, Zang, Yuepeng, Wang, Zheng, Huang, Shuai, Li, Xin, Datla, Raju, Fobert, Pierre R, Wang, Hong, Wei, Yangdou, Xiao, Wei
Format:	Online-Aufsatz
Sprache:	English
Veröffentlicht:	2019
Zugriff auf das übergeordnete Werk:	The New phytologist
Schlagworte:	Journal Article Research Support, Non-U.S. Gov't Arabidopsis thaliana cell death disease resistance low-temperature stress ubiquitination Arabidopsis Proteins F-Box Proteins SNC1 protein, Arabidopsis mehr... UBC13A protein, Arabidopsis EC 2.3.2.23 UBC13B protein, Arabidopsis Ubiquitin-Conjugating Enzymes Salicylic Acid O414PZ4LPZ

Beschreibung
Zusammenfassung:	© 2018 The Authors. New Phytologist © 2018 New Phytologist Trust. UBC13 is required for Lys63-linked polyubiquitination and innate immune responses in mammals, but its functions in plant immunity remain to be defined. Here we used genetic and pathological methods to evaluate roles of Arabidopsis UBC13 in response to pathogens and environmental stresses. Loss of UBC13 failed to activate the expression of numerous cold-responsive genes and resulted in hypersensitivity to low-temperature stress, indicating that UBC13 is involved in plant response to low-temperature stress. Furthermore, the ubc13 mutant displayed low-temperature-induced and salicylic acid-dependent lesion mimic phenotypes. Unlike typical lesion mimic mutants, ubc13 did not enhance disease resistance against virulent bacterial and fungal pathogens, but diminished hypersensitive response and compromised effector-triggered immunity against avirulent bacterial pathogens. UBC13 differently regulates two types of programmed cell death in response to low temperature and pathogen. The lesion mimic phenotype in the ubc13 mutant is partially dependent on SNC1. UBC13 interacts with an F-box protein CPR1 that regulates the homeostasis of SNC1. However, the SNC1 protein level was not altered in the ubc13 mutant, implying that UBC13 is not involved in CPR1-regulated SNC1 protein degradation. Taken together, our results revealed that UBC13 is a key regulator in plant response to low temperature and pathogens
Beschreibung:	Date Completed 18.02.2020 Date Revised 30.09.2020 published: Print-Electronic Citation Status MEDLINE
ISSN:	1469-8137
DOI:	10.1111/nph.15435