CPK28-NLP7 module integrates cold-induced Ca2+ signal and transcriptional reprogramming in Arabidopsis

被引:82
作者
Ding, Yanglin [1 ]
Yang, Hao [1 ]
Wu, Shifeng [1 ]
Fu, Diyi [1 ]
Li, Minze [1 ]
Gong, Zhizhong [1 ,2 ]
Yang, Shuhua [1 ]
机构
[1] China Agr Univ, Coll Biol Sci, State Key Lab Plant Physiol & Biochem, Beijing 100193, Peoples R China
[2] Hebei Univ, Sch Life Sci, Inst Life Sci & Green Dev, Baoding 071002, Hebei, Peoples R China
基金
中国国家自然科学基金;
关键词
LOW-TEMPERATURE; STRESS RESPONSES; PLANT-RESPONSES; FREEZING TOLERANCE; GENE-EXPRESSION; 14-3-3; PROTEINS; READ ALIGNMENT; SALICYLIC-ACID; IMMUNE; PHOSPHORYLATION;
D O I
10.1126/sciadv.abn7901
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Exposure to cold triggers a spike in cytosolic calcium (Ca2+) that often leads to transcriptional reprogramming in plants. However, how this Ca2+ signal is perceived and relayed to the downstream cold signaling pathway remains unknown. Here, we show that the CALCIUM-DEPENDENT PROTEIN KINASE 28 (CPK28) initiates a phosphorylation cascade to specify transcriptional reprogramming downstream of cold-induced Ca2+ signal. Plasma membrane (PM)-localized CPK28 is activated rapidly upon cold shock within 10 seconds in a Ca2+-dependent manner. CPK28 then phosphorylates and promotes the nuclear translocation of NIN-LIKE PROTEIN 7 (NLP7), a transcription factor that specifies the transcriptional reprogramming of cold-responsive gene sets in response to Ca2+, thereby positively regulating plant response to cold stress. This study elucidates a previously unidentified mechanism by which the CPK28-NLP7 regulatory module integrates cold-evoked Ca2+ signal and transcriptome and thus uncovers a key strategy for the rapid perception and transduction of cold signals from the PM to the nucleus.
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页数:17
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