Loss-of-function of Arabidopsis receptor-like kinase BIR1 activates cell death and defense responses mediated by BAK1 and SOBIR1
© 2016 The Authors. New Phytologist © 2016 New Phytologist Trust.
| Veröffentlicht in: | The New phytologist. - 1979. - 212(2016), 3 vom: 19. Nov., Seite 637-645 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2016
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| Zugriff auf das übergeordnete Werk: | The New phytologist |
| Schlagworte: | Journal Article BAK1-INTERACTING RECEPTOR-LIKE KINASE 1 (BIR1) BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED RECEPTOR KINASE 1 (BAK1) SUPPRESSOR OF BIR1-1 1 (SOBIR1) cell death plant immunity receptor-like kinase Arabidopsis Proteins Reactive Oxygen Species Flagellin mehr... |
| Zusammenfassung: | © 2016 The Authors. New Phytologist © 2016 New Phytologist Trust. The Arabidopsis receptor-like kinase (RLK) BIR1 (BAK1-INTERACTING RECEPTOR-LIKE KINASE 1) functions as a negative regulator of plant immunity. Previous work showed that loss-of-function of BIR1 leads to constitutive activation of cell death and defense responses. These autoimmune phenotypes are partially dependent on another RLK, SOBIR1. In order to identify additional components involved in the BIR1-regulated plant defense signaling pathway, a suppressor screen was carried out in the bir1-1 pad4-1 mutant background. Mutations in the suppressor mutants were identified by genetic mapping and re-sequencing of the mutant genomes. A number of suppressor mutants were found to carry mutations in an additional RLK, BAK1, indicating that BAK1 is required for activation of cell death and defense responses in bir1-1. Co-immunoprecipitation analysis revealed that BAK1 and SOBIR1 associate with each other in planta when the function of BIR1 is compromised. Although BAK1 was previously characterized as a negative regulator of cell death, our study highlights a novel role of BAK1 in promoting cell death and defense responses in conjunction with SOBIR1 |
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| Beschreibung: | Date Completed 26.01.2018 Date Revised 04.12.2021 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1469-8137 |
| DOI: | 10.1111/nph.14072 |