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The molecular basis of cold\u2010activated immunity was therefore investigated in\n                    <jats:styled-content style=\"fixed-case\">\n                      <jats:italic>Arabidopsis thaliana<\/jats:italic>\n                    <\/jats:styled-content>\n                    inoculated with the bacterial pathogen\n                    <jats:italic>Pst<\/jats:italic>\n                    DC3000, using a transcriptomic analysis. Exposure to cold stress for 10\u00a0hr was sufficient to activate immunity, as well as H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    accumulation and callose deposition. Transcriptome changes induced by the 10\u2010hr cold treatment were similar to those caused by pathogen infection, including increased expression of the salicylic acid (SA) pathway marker genes,\n                    <jats:italic>PR2<\/jats:italic>\n                    and\n                    <jats:italic>PR5<\/jats:italic>\n                    , and genes playing positive roles in defence against (hemi)\u2010biotrophs. In contrast, transcripts encoding jasmonic acid (JA) pathway markers such as\n                    <jats:italic>PR4<\/jats:italic>\n                    and\n                    <jats:italic>MYC2<\/jats:italic>\n                    and transcripts with positive roles in defence against necrotrophs were less abundant following the 10\u2010hr cold treatment. Cold\u2010activated immunity was dependent on SA, being partially dependent on\n                    <jats:italic>NPR1<\/jats:italic>\n                    and\n                    <jats:italic>ICS1<\/jats:italic>\n                    \/\n                    <jats:italic>SID2<\/jats:italic>\n                    . In addition, transcripts encoding SA biosynthesis enzymes such as ICS2, PAL1, PAL2, and PAL4 (but not ICS1\/SID2) and MES9 were more abundant, whereas\n                    <jats:italic>GH3.5<\/jats:italic>\n                    \/\n                    <jats:italic>WES1<\/jats:italic>\n                    and\n                    <jats:italic>SOT12<\/jats:italic>\n                    transcripts that encode components involved in SA modification were less abundant following cold stress treatment. These findings show that cold stress cross\u2010activates innate immune responses via a SA\u2010dependent pathway.\n                  <\/jats:p>","DOI":"10.1111\/pce.13579","type":"journal-article","created":{"date-parts":[[2019,5,13]],"date-time":"2019-05-13T20:03:48Z","timestamp":1557777828000},"page":"2645-2663","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":108,"title":["Cold stress activates disease resistance in\n                    <scp>\n                      <i>Arabidopsis thaliana<\/i>\n                    <\/scp>\n                    through a salicylic acid dependent pathway"],"prefix":"10.1111","volume":"42","author":[{"given":"Zhenjiang","family":"Wu","sequence":"first","affiliation":[{"name":"School of Life Sciences Central China Normal University  Wuhan 43009 P.R. 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China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yizhong","family":"Wang","sequence":"additional","affiliation":[{"name":"School of Life Sciences Central China Normal University  Wuhan 43009 P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ye","family":"Jin","sequence":"additional","affiliation":[{"name":"School of Life Sciences Central China Normal University  Wuhan 43009 P.R. China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huazhong","family":"Shi","sequence":"additional","affiliation":[{"name":"School of Life Sciences Central China Normal University  Wuhan 43009 P.R. 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