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The chemical \u03b2\u2010aminobutyric acid (\n BABA<\/jats:styled-content>\n ) enhances\n \n A<\/jats:styled-content>\n rabidopsis thaliana\n <\/jats:italic>\n resistance to hemibiotrophic bacteria through the priming of the salicylic acid (\n SA<\/jats:styled-content>\n ) defence response. Whether\n BABA<\/jats:styled-content>\n increases\n A<\/jats:styled-content>\n rabidopsis resistance to the necrotrophic bacterium\n \n P<\/jats:styled-content>\n ectobacterium carotovorum\n <\/jats:italic>\n ssp\n . carotovorum<\/jats:italic>\n (\n \n P<\/jats:styled-content>\n cc\n <\/jats:italic>\n ) is not clear. In this work, we show that treatment with\n BABA<\/jats:styled-content>\n protects\n A<\/jats:styled-content>\n rabidopsis against the soft\u2010rot pathogen\n \n P<\/jats:styled-content>\n cc\n <\/jats:italic>\n .\n BABA<\/jats:styled-content>\n did not prime the expression of the jasmonate\/ethylene\u2010responsive gene\n PLANT DEFENSIN 1.2<\/jats:italic>\n (\n \n PDF<\/jats:styled-content>\n 1.2\n <\/jats:italic>\n ), the up\u2010regulation of which is usually associated with resistance to necrotrophic pathogens. Expression of the\n SA<\/jats:styled-content>\n marker gene\n PATHOGENESIS RELATED 1<\/jats:italic>\n (\n \n PR<\/jats:styled-content>\n 1\n <\/jats:italic>\n ) on\n \n P<\/jats:styled-content>\n cc\n <\/jats:italic>\n infection was primed by\n BABA<\/jats:styled-content>\n treatment, but\n SA<\/jats:styled-content>\n \u2010defective mutants demonstrated a wild\u2010type level of\n BABA<\/jats:styled-content>\n \u2010induced resistance against\n Pcc<\/jats:italic>\n . BABA primed the expression of the pattern\u2010triggered immunity (PTI)\u2010responsive genes\n FLG22\u2010INDUCED RECEPTOR\u2010LIKE KINASE 1<\/jats:italic>\n (\n FRK1<\/jats:italic>\n ),\n ARABIDOPSIS NON\u2010RACE SPECIFIC DISEASE RESISTANCE GENE (NDR1)\/HAIRPIN\u2010INDUCED GENE (HIN1)\u2010LIKE 10<\/jats:italic>\n (\n NHL10<\/jats:italic>\n ) and\n CYTOCHROME P450, FAMILY 81<\/jats:italic>\n (\n CYP81F2<\/jats:italic>\n ) after inoculation with\n \n P<\/jats:styled-content>\n cc\n <\/jats:italic>\n or after treatment with purified bacterial microbe\u2010associated molecular patterns, such as flg22 or elf26.\n PTI<\/jats:styled-content>\n \u2010mediated callose deposition was also potentiated in\n BABA<\/jats:styled-content>\n \u2010treated\n A<\/jats:styled-content>\n rabidopsis, and\n BABA<\/jats:styled-content>\n boosted\n A<\/jats:styled-content>\n rabidopsis stomatal immunity to\n \n P<\/jats:styled-content>\n cc\n <\/jats:italic>\n .\n BABA<\/jats:styled-content>\n treatment primed the\n PTI<\/jats:styled-content>\n response in the\n SA<\/jats:styled-content>\n \u2010defective mutants\n SA induction deficient 2\u20101<\/jats:italic>\n (\n sid2\u20101<\/jats:italic>\n ) and\n phytoalexin deficient 4\u20101<\/jats:italic>\n (\n pad4\u20101<\/jats:italic>\n ). In addition,\n BABA<\/jats:styled-content>\n priming was associated with open chromatin configurations in the promoter region of\n PTI<\/jats:styled-content>\n marker genes. Our data indicate that\n BABA<\/jats:styled-content>\n primes the\n PTI<\/jats:styled-content>\n response upon necrotrophic bacterial infection and suggest a role for the\n PTI<\/jats:styled-content>\n response in\n BABA<\/jats:styled-content>\n \u2010induced resistance.\n <\/jats:p>","DOI":"10.1111\/j.1364-3703.2012.00827.x","type":"journal-article","created":{"date-parts":[[2012,9,4]],"date-time":"2012-09-04T22:21:21Z","timestamp":1346797281000},"page":"58-70","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":88,"title":["Priming of the\n A<\/scp>\n rabidopsis pattern\u2010triggered immunity response upon infection by necrotrophic\n \n P<\/scp>\n ectobacterium carotovorum\n <\/i>\n bacteria"],"prefix":"10.1111","volume":"14","author":[{"given":"Chen","family":"Po\u2010Wen","sequence":"first","affiliation":[{"name":"Department of Life Science and Institute of Plant Biology National Taiwan University Rm 1150, Life Science 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