4.7 Article

ALKBH9C, a potential RNA m6A demethylase, regulates the response of Arabidopsis to abiotic stresses and abscisic acid

Journal

PLANT CELL AND ENVIRONMENT
Volume 45, Issue 12, Pages 3566-3581

Publisher

WILEY
DOI: 10.1111/pce.14447

Keywords

epitranscriptomics; RNA demethylation

Categories

Funding

  1. NRF of Korea
  2. New Breeding Technologies Development Programme

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This study investigates the function of ALKBH9C protein in seed germination and seedling growth in Arabidopsis thaliana under abiotic stress and ABA conditions. The results suggest that ALKBH9C acts as an m(6)A eraser and plays a crucial role in seed germination and seedling growth under abiotic stresses or ABA by affecting the stability of stress-responsive transcripts.
Although several studies have shown that AlkB homolog (ALKBH) proteins are potential RNA demethylases (referred to as 'erasers'), biological functions of only a few ALKBH proteins have been characterized to date. In this study, we determined the function of ALKBH9C (At4g36090) in seed germination and seedling growth of Arabidopsis thaliana in response to abiotic stress and abscisic acid (ABA). Seed germination of the alkbh9c mutant was delayed in response to salt, drought, cold and ABA. Moreover, seedling growth of the mutant was repressed under salt stress or ABA but enhanced under drought conditions. Notably, the stress-responsive phenotypes were associated with the altered expression of several m(6)A-modified transcripts related to salt, drought or ABA response. Global m(6)A levels were increased in the alkbh9c mutant, and ALKBH9C bound to m(6)A-modified RNAs and had in vitro m(6)A demethylase activity, suggesting its potential role as an m(6)A eraser. The m(6)A levels in several stress-responsive genes were increased in the alkbh9c mutant, and the stability of m(6)A-modified transcripts was altered in the mutant. Collectively, our results suggest that m(6)A eraser ALKBH9C is crucial for seed germination and seedling growth of Arabidopsis in response to abiotic stresses or ABA via affecting the stability of stress-responsive transcripts.

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