The NAC transcription factor MdNAC4 positively regulates nitrogen deficiency-induced leaf senescence by enhancing ABA biosynthesis in apple

Although it is well established that nitrogen (N) deficiency induces leaf senescence, the molecular mechanism of N deficiency-induced leaf senescence remains largely unknown. Here, we show that an abscisic acid (ABA)-responsive NAC transcription factor (TF) is involved in N deficiency-induced leaf s...

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Bibliographic Details
Published in:Molecular horticulture 2023-03, Vol.3 (1), p.5-20, Article 5
Main Authors: Wen, Binbin, Zhao, Xuehui, Gong, Xingyao, Zhao, Wenzhe, Sun, Mingyue, Chen, Xiude, Li, Dongmei, Li, Ling, Xiao, Wei
Format: Article
Language:English
Subjects:
ABA
Abscisic acid
Apple
Biosynthesis
Gene expression
Hormones
Kinases
Leaf senescence
MdNAC4
MdPYL4
Metabolism
N deficiency
Nutrients
Phosphatase
Proteins
Senescence
Signal transduction
Transcription factors
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Summary:Although it is well established that nitrogen (N) deficiency induces leaf senescence, the molecular mechanism of N deficiency-induced leaf senescence remains largely unknown. Here, we show that an abscisic acid (ABA)-responsive NAC transcription factor (TF) is involved in N deficiency-induced leaf senescence. The overexpression of MdNAC4 led to increased ABA levels in apple calli by directly activating the transcription of the ABA biosynthesis gene MdNCED2. In addition, MdNAC4 overexpression promoted N deficiency-induced leaf senescence. Further investigation showed that MdNAC4 directly bound the promoter of the senescence-associated gene (SAG) MdSAG39 and upregulated its expression. Interestingly, the function of MdNAC4 in promoting N deficiency-induced leaf senescence was enhanced in the presence of ABA. Furthermore, we identified an interaction between the ABA receptor protein MdPYL4 and the MdNAC4 protein. Moreover, MdPYL4 showed a function similar to that of MdNAC4 in ABA-mediated N deficiency-induced leaf senescence. These findings suggest that ABA plays a central role in N deficiency-induced leaf senescence and that MdPYL4 interacts with MdNAC4 to enhance the response of the latter to N deficiency, thus promoting N deficiency-induced leaf senescence. In conclusion, our results provide new insight into how MdNAC4 regulates N deficiency-induced leaf senescence.
ISSN:2730-9401
2730-9401
DOI:10.1186/s43897-023-00053-4