The antisense CircRNA VvcircABH controls salt tolerance and the brassinosteroid signaling response by suppressing cognate mRNA splicing in grape

Soil salinization is a major factor limiting the sustainable development of the grape industry. Circular RNAs (circRNAs) are more stable than linear mRNAs and are involved in stress responses. However, the biological functions and molecular mechanisms underlying antisense circRNAs in plants remain u...

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Veröffentlicht in:The New phytologist 2024-12
Hauptverfasser: Gao, Zhen, Su, Yifan, Wang, Yaru, Li, Yeqi, Wu, Yue, Sun, Xinru, Yao, Yuxin, Ma, Chao, Li, Jing, Du, Yuanpeng
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Sprache:eng
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Zusammenfassung:Soil salinization is a major factor limiting the sustainable development of the grape industry. Circular RNAs (circRNAs) are more stable than linear mRNAs and are involved in stress responses. However, the biological functions and molecular mechanisms underlying antisense circRNAs in plants remain unclear. We identified the antisense circRNA VvcircABH through high-throughput sequencing. Using genetic transformation methods and molecular biological techniques, we analyzed the effects of VvcircABH on the response to salt stress and the mechanisms underlying its effects. VvcircABH was located in the nucleus and upregulated by salt stress, while the expression level of its cognate gene VvABH (alpha/beta-hydrolase) was downregulated. VvcircABH overexpression or VvABH silencing greatly enhanced grape salt tolerance. VvcircABH could bind to the overlapping region and inhibits VvABH pre-mRNA splicing, thereby decreasing the expression level of VvABH. Additionally, VvcircABH repressed the additive effect of VvABH on the interaction between VvBRI1 (brassinosteroid-insensitive 1) and VvBKI1 (BRI1 kinase inhibitor 1), thus influencing the plant's response to BR, which plays important roles in plant salt tolerance. We conclude that VvcircABH and VvABH play distinct roles in the salt tolerance and brassinosteroid signaling response, and VvcircABH could govern the expression of VvABH by inhibiting its splicing.
ISSN:1469-8137
1469-8137
DOI:10.1111/nph.20306