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Cold stress activates disease resistance in Arabidopsis thaliana through a salicylic acid dependent pathway
Author(s) -
Wu Zhenjiang,
Han Shiming,
Zhou Hedan,
Tuang Za Khai,
Wang Yizhong,
Jin Ye,
Shi Huazhong,
Yang Wannian
Publication year - 2019
Publication title -
plant, cell and environment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.646
H-Index - 200
eISSN - 1365-3040
pISSN - 0140-7791
DOI - 10.1111/pce.13579
Subject(s) - jasmonic acid , biology , salicylic acid , transcriptome , callose , arabidopsis thaliana , plant disease resistance , innate immune system , arabidopsis , npr1 , gene , microbiology and biotechnology , genetics , gene expression , immune system , mutant , medicine , heart failure , natriuretic peptide
Exposure to short‐term cold stress influences disease resistance by mechanisms that remain poorly characterized. The molecular basis of cold‐activated immunity was therefore investigated in Arabidopsis thaliana inoculated with the bacterial pathogen Pst DC3000, using a transcriptomic analysis. Exposure to cold stress for 10 hr was sufficient to activate immunity, as well as H 2 O 2 accumulation and callose deposition. Transcriptome changes induced by the 10‐hr cold treatment were similar to those caused by pathogen infection, including increased expression of the salicylic acid (SA) pathway marker genes, PR2 and PR5 , and genes playing positive roles in defence against (hemi)‐biotrophs. In contrast, transcripts encoding jasmonic acid (JA) pathway markers such as PR4 and MYC2 and transcripts with positive roles in defence against necrotrophs were less abundant following the 10‐hr cold treatment. Cold‐activated immunity was dependent on SA, being partially dependent on NPR1 and ICS1 / SID2 . In addition, transcripts encoding SA biosynthesis enzymes such as ICS2, PAL1, PAL2, and PAL4 (but not ICS1/SID2) and MES9 were more abundant, whereas GH3.5 / WES1 and SOT12 transcripts that encode components involved in SA modification were less abundant following cold stress treatment. These findings show that cold stress cross‐activates innate immune responses via a SA‐dependent pathway.