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ALKBH8B, a Putative RNA Demethylase, Plays a Role in the Response of Arabidopsis to Salt Stress and Abscisic Acid

机译:ALKBH8B, a Putative RNA Demethylase, Plays a Role in the Response of Arabidopsis to Salt Stress and Abscisic Acid

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Abstract RNA methylation and demethylation, which are mediated by RNA methyltransferases (referred to as “writers”) and demethylases (referred to as “erasers”), respectively, have increasingly been demonstrated to play crucial roles in stress responses as well as in plant development. The Arabidopsis thaliana genome encodes thirteen AlkB homolog (ALKBH) proteins that are potential RNA demethylases; however, the functions of most ALKBHs are yet to be determined. In this study, we characterized the function of a potential eraser protein ALKBH8B (At4g02485) during seed germination and seedling growth of Arabidopsis under abiotic stresses. Confocal analysis of the ALKBH8B-GFP expression confirmed that ALKBH8B is localized in the nucleus. The loss-of-function alkbh8b mutant exhibited no apparent phenotypes compared with the wild type under normal and abiotic stress conditions. In contrast, the ALKBH8B-overexpressing transgenic Arabidopsis plants displayed salt-tolerant phenotypes exhibiting better seedling growth and survival rate than wild-type under salt stress. Notably, salt tolerance of the transgenic plants was associated with up- and down-regulation of the expression of several m6A-modified salt stress positive and negative regulators, respectively. Moreover, cotyledon greening and seedling growth of the ALKBH8B-overexpressing transgenic plants were much higher than those of wild type upon abscisic acid (ABA) application, and the transcript levels of ABA signaling-related genes, such as ABI3 and ABI4 were markedly decreased in the transgenic plants. Importantly, global m6A levels decreased in the ALKBH8B-overexpressing transgenic plants as compared with the wild type. Collectively, these results indicate that ALKBH8B plays a role in the response of Arabidopsis to salt stress and ABA via modulating the expression of salt stress- or ABA signaling-related genes.

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