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Li, Lei

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Li, Lei
Author's Publications: search.filters.isAuthorOfPublication.15515771-5a68-4ef6-97ba-dfe254c00bd4

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    Glc-TOR signalling leads transcriptome reprogramming and meristem activation
    (2013) Xiong, Yan; McCormack, Matthew; Li, Lei; Hall, Qi; Xiang, Chengbin; Sheen, Jen
    Meristems encompass stem/progenitor cells that sustain postembryonic growth of all plant organs. How meristems are activated and sustained by nutrient signalling remains enigmatic in photosynthetic plants. Combining chemical manipulations and chemical genetics at the photoautotrophic transition checkpoint, we reveal that shoot photosynthesis-derived glucose drives target-of-rapamycin (TOR) signalling relays through glycolysis and mitochondrial bioenergetics to control root meristem activation, which is decoupled from direct glucose sensing, growth-hormone signalling, and stem-cell maintenance. Surprisingly, glucose-TOR signalling dictates transcriptional reprogramming of remarkable gene sets involved in central and secondary metabolism, cell cycle, transcription, signalling, transport and folding. Systems, cellular and genetic analyses uncover TOR phosphorylation of E2Fa transcription factor for an unconventional activation of S-phase genes, and glucose-signalling defects in e2fa root meristems. Our findings establish pivotal roles of glucose-TOR signalling in unprecedented transcriptional networks wiring central metabolism and biosynthesis for energy and biomass production, and integrating localized stem/progenitor-cell proliferation through inter-organ nutrient coordination to control developmental transition and growth.
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    RD26 mediates crosstalk between drought and brassinosteroid signalling pathways
    (Nature Publishing Group, 2017) Ye, Huaxun; Liu, Sanzhen; Tang, Buyun; Chen, Jiani; Xie, Zhouli; Nolan, Trevor M.; Jiang, Hao; Guo, Hongqing; Lin, Hung-Ying; Li, Lei; Wang, Yanqun; Tong, Hongning; Zhang, Mingcai; Chu, Chengcai; Li, Zhaohu; Aluru, Maneesha; Aluru, Srinivas; Schnable, Patrick S.; Yin, Yanhai
    Brassinosteroids (BRs) regulate plant growth and stress responses via the BES1/BZR1 family of transcription factors, which regulate the expression of thousands of downstream genes. BRs are involved in the response to drought, however the mechanistic understanding of interactions between BR signalling and drought response remains to be established. Here we show that transcription factor RD26 mediates crosstalk between drought and BR signalling. When overexpressed, BES1 target gene RD26 can inhibit BR-regulated growth. Global gene expression studies suggest that RD26 can act antagonistically to BR to regulate the expression of a subset of BES1-regulated genes, thereby inhibiting BR function. We show that RD26 can interact with BES1 protein and antagonize BES1 transcriptional activity on BR-regulated genes and that BR signalling can also repress expression of RD26 and its homologues and inhibit drought responses. Our results thus reveal a mechanism coordinating plant growth and drought tolerance.
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    Bifurcation of Arabidopsis NLR Immune Signaling via Ca2+-Dependent Protein Kinases
    (Public Library of Science, 2013) Gao, Xiquan; Chen, Xin; Lin, Wenwei; Chen, Sixue; Lu, Dongping; Niu, Yajie; Li, Lei; Cheng, Cheng; McCormack, Matthew; Sheen, Jenq-Yunn; Shan, Libo; He, Ping
    Nucleotide-binding domain leucine-rich repeat (NLR) protein complexes sense infections and trigger robust immune responses in plants and humans. Activation of plant NLR resistance (R) proteins by pathogen effectors launches convergent immune responses, including programmed cell death (PCD), reactive oxygen species (ROS) production and transcriptional reprogramming with elusive mechanisms. Functional genomic and biochemical genetic screens identified six closely related Arabidopsis Ca2+-dependent protein kinases (CPKs) in mediating bifurcate immune responses activated by NLR proteins, RPS2 and RPM1. The dynamics of differential CPK1/2 activation by pathogen effectors controls the onset of cell death. Sustained CPK4/5/6/11 activation directly phosphorylates a specific subgroup of WRKY transcription factors, WRKY8/28/48, to synergistically regulate transcriptional reprogramming crucial for NLR-dependent restriction of pathogen growth, whereas CPK1/2/4/11 phosphorylate plasma membrane-resident NADPH oxidases for ROS production. Our studies delineate bifurcation of complex signaling mechanisms downstream of NLR immune sensors mediated by the myriad action of CPKs with distinct substrate specificity and subcellular dynamics.