The HcABF2-HcFIP37-HcPYL2 module regulates salt tolerance via the ABA signaling pathways in kenaf (Hibiscus cannabinus L.).

Authors

Caijin Wang, Yan Liu, Dengjie Luo, Rehmat Ullah, Jiao Yue, Huaming Lu, Ru Li, Peng Chen

Published in

Plant physiology. Jul 24, 2026. Epub Jul 24, 2026.

Abstract

N6-methyladenosine (m6A), a key epigenetic post-transcriptional modification, plays a critical role in regulating gene expression and mRNA stability. However, its functional mechanisms in mediating plant adaptation to abiotic stresses remain largely unexplored. Here, we demonstrate that HcFIP37 is a member of the m6A methyltransferase family in kenaf and that it possesses m6A methylation activity. Functional characterization showed that HcFIP37 overexpression significantly increased global m6A levels and enhanced kenaf salt tolerance, while its silencing had opposite effects. We further found that HcFIP37 expression was inducible by the plant hormone abscisic acid (ABA), and identified HcABF2, a core regulatory component of the ABA signaling pathway, as the key transcription factor responsible for the activation of HcFIP37 expression. Additionally, analysis indicated that the interaction of HcHB7 with HcFIP37 promoted the protein stability of HcFIP37 and enhances the ability of HcFIP37 to bind the canonical m6A motifs (RRACH and UGUAY). To elucidate the downstream effects, virus induced gene silencing (VIGS) of HcFIP37 triggered global transcriptional reprogramming, and RNA-seq identified 3066 differentially expressed transcripts (DETs). Mechanistically, HcFIP37 binds to the canonical m6A motif (RRACH) within HcPYL2 mRNA, enhancing both its transcript stability and translation efficiency. Genetic analyses confirmed that HcPYL2 functions downstream of HcFIP37. Collectively, our findings demonstrate that the m6A methyltransferase HcFIP37 serves as a core mediator of kenaf salt tolerance, which integrates the ABA signaling by regulating mRNA stability, defining a novel HcABF2-HcFIP37-HcPYL2 regulatory pathway.

PMID:
42497309
Bibliographic data and abstract were imported from PubMed on 25 Jul 2026.

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