Hijacking of the jasmonate pathway by the mycotoxin fumonisin B1 (FB1) to initiate programmed cell death in Arabidopsis is modulated by RGLG3 and RGLG4

Hijacking of the jasmonate pathway by the mycotoxin fumonisin B1 (FB1) to initiate programmed cell death in Arabidopsis is modulated by RGLG3 and RGLG4

© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.

Bibliographische Detailangaben
Veröffentlicht in:Journal of experimental botany. - 1985. - 66(2015), 9 vom: 18. Mai, Seite 2709-21
1. Verfasser: Zhang, Xu (VerfasserIn)
Weitere Verfasser: Wu, Qian, Cui, Shao, Ren, Jiao, Qian, Wanqiang, Yang, Yang, He, Shanping, Chu, Jinfang, Sun, Xiaohong, Yan, Cunyu, Yu, Xiangchun, An, Chengcai
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Journal of experimental botany
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Arabidopsis RGLG3 RGLG4 fumonisin B1 jasmonate programmed cell death salicylic acid. Arabidopsis Proteins mehr... Cyclopentanes Fumonisins Oxylipins 3ZZM97XZ32 jasmonic acid 6RI5N05OWW Ligases EC 6.- RGLG3 protein, Arabidopsis RGLG4 protein, Arabidopsis Salicylic Acid O414PZ4LPZ
Beschreibung
Zusammenfassung:© The Author 2015. Published by Oxford University Press on behalf of the Society for Experimental Biology.
The mycotoxin fumonisin B1 (FB1) is a strong inducer of programmed cell death (PCD) in plants, but its underlying mechanism remains unclear. Here, we describe two ubiquitin ligases, RING DOMAIN LIGASE3 (RGLG3) and RGLG4, which control FB1-triggered PCD by modulating the jasmonate (JA) signalling pathway in Arabidopsis thaliana. RGLG3 and RGLG4 transcription was sensitive to FB1. Arabidopsis FB1 sensitivity was suppressed by loss of function of RGLG3 and RGLG4 and was increased by their overexpression. Thus RGLG3 and RGLG4 have coordinated and positive roles in FB1-elicited PCD. Mutated JA perception by coi1 disrupted the RGLG3- and RGLG4-related response to FB1 and interfered with their roles in cell death. Although FB1 induced JA-responsive defence genes, it repressed growth-related, as well as JA biosynthesis-related, genes. Consistently, FB1 application reduced JA content in wild-type plants. Furthermore, exogenously applied salicylic acid additively suppressed JA signalling with FB1 treatment, suggesting that FB1-induced salicylic acid inhibits the JA pathway during this process. All of these effects were attenuated in rglg3 rglg4 plants. Altogether, these data suggest that the JA pathway is hijacked by the toxin FB1 to elicit PCD, which is coordinated by Arabidopsis RGLG3 and RGLG4
Beschreibung:Date Completed 09.02.2016
Date Revised 16.03.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1460-2431
DOI:10.1093/jxb/erv068