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MYB47 delays leaf senescence by modulating jasmonate pathway via direct regulation of CYP94B3 / CYP94C1 expression in Arabidopsis
Author(s) -
Cao Jie,
Yang Qi,
Zhao Yaning,
Tan Shuya,
Li Shichun,
Cheng Dawei,
Zhang Ruxue,
Zhang Murao,
Li Zhonghai
Publication year - 2025
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.70133
Summary Leaf senescence is a complex genetic process intricately regulated by multiple layers of control. Transcription factors, as master regulators of gene expression, play crucial roles in initiating and progressing leaf senescence. Through screening an activation‐tagged mutant library, we identified MYB47 as a negative regulator of leaf senescence. Constitutive or inducible overexpression of MYB47 significantly delays leaf senescence, while loss‐of‐function mutants exhibit accelerated senescence. Transcriptome analysis revealed a marked suppression of jasmonic acid (JA) signaling in MYB47 overexpression lines. Conversely, the myb47 mutants display elevated JA levels and reduced expression of JA catabolic genes, CYP94B3 and CYP94C1 . Biochemical evidence demonstrated that MYB47 directly binds to the promoters of CYP94B3 and CYP94C1 , upregulating their expression. Consequently, JA contents are significantly reduced in MYB47 overexpression lines. Overexpressing CYP94B3 or CYP94C1 in myb47 mutants alleviates their early senescence phenotype. Furthermore, JA induces MYB47 expression, forming a negative feedback loop (JA‐MYB47‐CYP94B3/C1‐JA) that fine‐tunes leaf senescence. Our findings reveal a novel regulatory module involving MYB47 and JA signaling that governs leaf senescence. By stimulating JA catabolism and attenuating JA signaling, MYB47 plays a crucial role in delaying leaf senescence.
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