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Arabidopsis SnRK1 negatively regulates phenylpropanoid metabolism via Kelch domain‐containing F‐box proteins
Author(s) -
Wang Bin,
Zhao Xianhai,
Zhao Yunjun,
Shanklin John,
Zhao Qiao,
Liu ChangJun
Publication year - 2021
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.17121
Subject(s) - phenylpropanoid , downregulation and upregulation , biochemistry , microbiology and biotechnology , arabidopsis , metabolism , phenylalanine ammonia lyase , bimolecular fluorescence complementation , biology , chemistry , biosynthesis , gene , enzyme , mutant , peroxidase
Summary Phenylpropanoid metabolism represents a substantial metabolic sink for photosynthetically fixed carbon. The evolutionarily conserved Sucrose Non‐Fermenting Related Kinase 1 (SnRK1) is a major metabolic sensor that reprograms metabolism upon carbon deprivation. However, it is not clear if and how the SnRK1‐mediated sugar signaling pathway controls phenylpropanoid metabolism. Here, we show that Arabidopsis SnRK1 negatively regulates phenylpropanoid biosynthesis via a group of Kelch domain‐containing F‐box (KFB) proteins that are responsible for the ubiquitination and degradation of phenylalanine ammonia lyase (PAL). Downregulation of AtSnRK1 significantly promoted the accumulation of soluble phenolics and lignin polymers and drastically increased PAL cellular accumulation but only slightly altered its transcription level. Co‐expression of SnRK1α with PAL in Nicotiana benthamiana leaves resulted in the severe attenuation of the latter’s protein level, but protein interaction assays suggested PAL is not a direct substrate of SnRK1. Furthermore, up or downregulation of AtSnRK1 positively affected KFB PAL s gene expression, and energy starvation upregulated KFB PAL expression, which partially depends on AtSnRK1. Collectively, our study reveals that SnRK1 negatively regulates phenylpropanoid biosynthesis, and KFB PALs act as regulatory components of the SnRK1 signaling network, transcriptionally regulated by SnRK1 and subsequently mediate proteasomal degradation of PAL in response to the cellular carbon availability.