Intronic microRNA-directed regulation of mitochondrial reactive oxygen species enhances plant stress tolerance in Arabidopsis
© 2023 The Authors New Phytologist © 2023 New Phytologist Foundation.
Veröffentlicht in: | The New phytologist. - 1979. - 240(2023), 2 vom: 15. Okt., Seite 710-726 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2023
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Zugriff auf das übergeordnete Werk: | The New phytologist |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't RNA splicing intron retain miRNA post-transcriptional regulation reactive oxygen species MicroRNAs Reactive Oxygen Species |
Zusammenfassung: | © 2023 The Authors New Phytologist © 2023 New Phytologist Foundation. MicroRNAs (miRNAs) play crucial roles in regulating plant development and stress responses. However, the functions and mechanism of intronic miRNAs in plants are poorly understood. This study reports a stress-responsive RNA splicing mechanism for intronic miR400 production, whereby miR400 modulates reactive oxygen species (ROS) accumulation and improves plant tolerance by downregulating its target expression. To monitor the intron splicing events, we used an intronic miR400 splicing-dependent luciferase transgenic line. Luciferase activity was observed to decrease after high cadmium concentration treatment due to the retention of the miR400-containing intron, which inhibited the production of mature miR400. Furthermore, we demonstrated that under Cd treatments, Pentatricopeptide Repeat Protein 1 (PPR1), the target of miR400, acts as a positive regulator by inducing ROS accumulation. Ppr1 mutation affected the Complex III activity in the electron transport chain and RNA editing of the mitochondrial gene ccmB. This study illustrates intron splicing as a key step in intronic miR400 production and highlights the function of intronic miRNAs as a 'signal transducer' in enhancing plant stress tolerance |
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Beschreibung: | Date Completed 22.09.2023 Date Revised 24.09.2023 published: Print-Electronic RefSeq: AT1G32583, AT1G06580, AT1G62720, AT1G08830, ATMG00110, GSE211873 Citation Status MEDLINE |
ISSN: | 1469-8137 |
DOI: | 10.1111/nph.19168 |