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Heightened resistance to one pathogen often coincides with increased susceptibility to another pathogen. However, the underlying molecular basis of this antagonistic response remains unclear.<\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Here, we demonstrate that mutants defective in the transcription factor\n                          <jats:italic>ETHYLENE\u2010INSENSITIVE 3\u2010LIKE 2<\/jats:italic>\n                          (\n                          <jats:italic>OsEIL2<\/jats:italic>\n                          ) exhibited enhanced resistance to the biotrophic bacterial pathogen\n                          <jats:italic>Xanthomonas oryzae<\/jats:italic>\n                          pv\n                          <jats:italic>oryzae<\/jats:italic>\n                          and to the hemibiotrophic fungal pathogen\n                          <jats:italic>Magnaporthe oryzae<\/jats:italic>\n                          , but enhanced susceptibility to the necrotrophic fungal pathogen\n                          <jats:italic>Rhizoctonia solani<\/jats:italic>\n                          .\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          Furthermore, necrotroph\u2010induced OsEIL2 binds to the promoter of\n                          <jats:italic>OsWRKY67<\/jats:italic>\n                          with high affinity, leading to the upregulation of salicylic acid (SA)\/jasmonic acid (JA) pathway genes and increased SA\/JA levels, ultimately resulting in enhanced resistance.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                      <jats:list-item>\n                        <jats:p>\n                          However, biotroph\u2010 and hemibiotroph\u2010induced OsEIL2 targets\n                          <jats:italic>OsERF083<\/jats:italic>\n                          , resulting in the inhibition of SA\/JA pathway genes and decreased SA\/JA levels, ultimately leading to reduced resistance. Our findings unveil a previously uncharacterized defense mechanism wherein two distinct transcriptional regulatory modules differentially mediate immunity against pathogens with different lifestyles through the transcriptional reprogramming of phytohormone pathway genes.\n                        <\/jats:p>\n                      <\/jats:list-item>\n                    <\/jats:list>\n                  <\/jats:p>","DOI":"10.1111\/nph.19809","type":"journal-article","created":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T23:36:40Z","timestamp":1715384200000},"page":"362-380","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["<scp>O<\/scp>\n                    s\n                    <scp>EIL<\/scp>\n                    2 balances rice immune responses against (hemi)biotrophic and necrotrophic pathogens via the salicylic acid and jasmonic acid 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