{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T05:02:55Z","timestamp":1785214975206,"version":"3.55.0"},"reference-count":50,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T00:00:00Z","timestamp":1783728000000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32500247"],"award-info":[{"award-number":["32500247"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007129","name":"Natural Science Foundation of Shandong Province","doi-asserted-by":"publisher","award":["ZR2024MC093"],"award-info":[{"award-number":["ZR2024MC093"]}],"id":[{"id":"10.13039\/501100007129","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["bsppjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Plant Pathology"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Calmodulin\u2010Binding Protein 60 (CBP60), a plant\u2010specific atypical transcription factor family, plays pivotal roles in reprogramming plant immunity. Loss of function of the CBP60b and CBP60b\/c\/d\/e\/f subfamily constitutively activates immune responses (autoimmunity). However, the specific mechanisms and pathways underlying this autoimmunity remain elusive. Here, through EMS mutagenesis of the\n                    <jats:italic>cbp60b<\/jats:italic>\n                    mutant, we isolated a dominant suppressor mutant that suppresses the\n                    <jats:italic>cbp60b<\/jats:italic>\n                    autoimmune phenotype. Sequencing identified a point mutation in\n                    <jats:italic>CBP60g<\/jats:italic>\n                    (designated\n                    <jats:italic>cbp60g\u20103<\/jats:italic>\n                    ) that causes an aspartate\u2010to\u2010asparagine substitution at position 252 and reduces its transcriptional activity. Increasing the expression of\n                    <jats:italic>CBP60g<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D252N<\/jats:italic>\n                    <\/jats:sup>\n                    restored the pathogen response defect of the\n                    <jats:italic>cbp60g;sard1<\/jats:italic>\n                    mutant. Strikingly, while wild\u2010type CBP60g failed to suppress the autoimmunity of\n                    <jats:italic>cbp60b<\/jats:italic>\n                    , the transcriptionally compromised CBP60g\n                    <jats:sup>D252N<\/jats:sup>\n                    variant completely suppressed it. Unexpectedly, we found that functional loss of canonical effector\u2010triggered immunity (ETI) pathways only partially suppressed the autoimmunity of the\n                    <jats:italic>cbp60b;c;d;e;f<\/jats:italic>\n                    quintuple mutant. Although simultaneously disrupting the ETI pathways and introducing CBP60g\n                    <jats:sup>D252N<\/jats:sup>\n                    further suppressed the autoimmunity of\n                    <jats:italic>cbp60b;c;d;e;f<\/jats:italic>\n                    , it still failed to achieve complete suppression. These results indicate that the autoimmunity in\n                    <jats:italic>cbp60b;c;d;e;f<\/jats:italic>\n                    mutant is mediated by both canonical ETI\u2010dependent and ETI\u2010independent pathways. These results provide new insights and raise further questions regarding the signalling mechanisms of plant autoimmunity.\n                  <\/jats:p>","DOI":"10.1111\/mpp.70318","type":"journal-article","created":{"date-parts":[[2026,7,11]],"date-time":"2026-07-11T07:13:26Z","timestamp":1783754006000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Canonical ETI\u2010Dependent and \u2010Independent Pathways Mediate Autoimmunity Caused by Loss of CBP60b Clade Function"],"prefix":"10.1111","volume":"27","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-7322-2658","authenticated-orcid":false,"given":"Lu\u2010Shen","family":"Li","sequence":"first","affiliation":[{"name":"College of Agriculture and Biology Liaocheng University  Liaocheng 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