Fe deficiency-induced ethylene synthesis confers resistance to Botrytis cinerea

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

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 237(2023), 5 vom: 06. März, Seite 1843-1855
1. Verfasser: Lu, Cheng Kai (VerfasserIn)
Weitere Verfasser: Liang, Gang
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2023
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Arabidopsis thaliana Botrytis cinerea FIT Fe deficiency ethylene pathogen Arabidopsis Proteins Basic Helix-Loop-Helix Transcription Factors Ethylenes
Beschreibung
Zusammenfassung:© 2022 The Authors New Phytologist © 2022 New Phytologist Foundation.
Although iron (Fe) deficiency is an adverse condition to growth and development of plants, it increases the resistance to pathogens. How Fe deficiency induces the resistance to pathogens is still unclear. Here, we reveal that the inoculation of Botrytis cinerea activates the Fe deficiency response of plants, which further induces ethylene synthesis and then resistance to B. cinerea. FIT and bHLH Ib are a pair of bHLH transcription factors, which control the Fe deficiency response. Both the Fe deficiency-induced ethylene synthesis and resistance are blocked in fit-2 and bhlh4x-1 (a quadruple mutant for four bHLH Ib members). SAM1 and SAM2, two ethylene synthesis-associated genes, are induced by Fe deficiency in a FIT-bHLH Ib-dependent manner. Moreover, SAM1 and SAM2 are required for the increased ethylene and resistance to B. cinerea under Fe-deficient conditions. Our findings suggest that the FIT-bHLH Ib module activates the expression of SAM1 and SAM2, thereby inducing ethylene synthesis and resistance to B. cinerea. This study uncovers that Fe signaling also functions as a part of the plant immune system against pathogens
Beschreibung:Date Completed 03.02.2023
Date Revised 08.02.2023
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.18638