Extracellular ATP targets Arabidopsis RIBONUCLEASE 1 to suppress mycotoxin stress-induced cell death

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

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 235(2022), 4 vom: 01. Aug., Seite 1531-1542
1. Verfasser: Goodman, Heather L (VerfasserIn)
Weitere Verfasser: Kroon, Johan T M, Tomé, Daniel F A, Hamilton, John M U, Alqarni, Ali O, Chivasa, Stephen
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 RNS1 S-like ribonuclease extracellular ATP fumonisin B1 programmed cell death salicylic acid Arabidopsis Proteins mehr... Mycotoxins Adenosine Triphosphate 8L70Q75FXE RNS1 protein, Arabidopsis EC 3.1.- Ribonucleases Salicylic Acid O414PZ4LPZ
Beschreibung
Zusammenfassung:© 2022 The Authors. New Phytologist © 2022 New Phytologist Foundation.
Extracellular ATP is a purinergic signal with important functions in regulating plant growth and stress-adaptive responses, including programmed cell death. While signalling events proximate to receptor activation at the plasma membrane have been characterised, downstream protein targets and the mechanism of cell death activation/regulation are unknown. We designed a proteomic screen to identify ATP-responsive proteins in Arabidopsis cell cultures exposed to mycotoxin stress via fumonisin B1 (FB1) application. Arabidopsis RIBONUCLEASE 1 (RNS1) was identified by the screen, and transgenic plants overexpressing native RNS1 showed greater susceptibility to FB1, while a gene knockout rns1 mutant and antisense RNS1 transgenic plants were resistant to FB1-induced cell death. Native RNS1 complemented rns1 mutants and restored the cell death response to FB1, while a catalytically inactive version of the ribonuclease could not. The FB1 resistance of salicylic acid (SA)-depleted nahG-expressing plants was abolished by transformation with native RNS1, but not the catalytically dead version. The mechanism of FB1-induced cell death is activation of RNS1-dependent RNA cleavage, which is blocked by ATP via RNS1 suppression, or enhanced by SA through induction of RNS1 expression. Our study reveals RNS1 as a previously unknown convergence point of ATP and SA signalling in the regulation of stress-induced cell death
Beschreibung:Date Completed 15.07.2022
Date Revised 15.10.2022
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.18211