| dc.contributor.advisor | Gatz, Christiane Prof. Dr. | |
| dc.contributor.author | Nair, Aswin | |
| dc.date.accessioned | 2021-03-25T14:36:26Z | |
| dc.date.available | 2021-03-25T14:36:26Z | |
| dc.date.issued | 2021-03-25 | |
| dc.identifier.uri | http://hdl.handle.net/21.11130/00-1735-0000-0008-57CB-2 | |
| dc.identifier.uri | http://dx.doi.org/10.53846/goediss-8517 | |
| dc.language.iso | eng | de |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | |
| dc.subject.ddc | 570 | de |
| dc.title | Salicylic Acid (SA)-independent processes in Systemic Acquired Resistance (SAR) | de |
| dc.type | doctoralThesis | de |
| dc.contributor.referee | Feussner, Ivo Prof. Dr. | |
| dc.date.examination | 2020-03-27 | |
| dc.description.abstracteng | SAR is an immune response that is established in the systemic leaves after infection of local leaves with biotrophic or hemibiotrophic pathogens. According to the current model, the amino acid-derived metabolite N-hydroxypipecolic acid (NHP) travels from the infected to the systemic leaf, where it induces the biosynthesis of salicylic acid (SA), resulting in a robust SAR response. Previous studies have shown that a subset of SAR related genes are induced even in the absence of SA biosynthesis, while gene induction is completely hampered in the absence of NHP biosynthesis. The purpose of this study was to decipher the SA-independent and NHP-dependent signalling cascade that activates gene expression during SAR. Using pharmacological treatment with NHP, we show that SAR-related genes such as FMO1, which encodes an enzyme involved in NHP biosynthesis, is induced even in the salicylic acid induction deficient 2 (sid2) mutant, which is devoid of pathogen-induced SA. The NHP-mediated induction of FMO1 required the SA receptor NON EXPRESSOR OF PATHOGENESIS-RELATED GENES1 (NPR1), and its interacting TGACG SEQUENCE-SPECIFIC BINDING PROTEIN (TGA) transcription factors. NHP treatment resulted in the accumulation of NPR1 protein in wild-type plants and to a lesser extent in the sid2 mutant. The structural similarity between SA and NHP prompted us to test if NHP binds to NPR1. Using isothermal titration calorimetry we show that while SA bound to NPR1 with a Kd value of 585 ± 368 nM, no binding to NHP was detected. Moreover, we show that the nucleocytoplasmic protein ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) was required for the NHP-induced expression of SAR-related genes. In this study, we show that NHP uses regulatory components of the SA signalling pathway to induce SAR genes, but the mechanism of its perception has remains an open question. | de |
| dc.contributor.coReferee | Polle, Andrea Prof. Dr. | |
| dc.contributor.thirdReferee | Wiermer, Marcel PD Dr. | |
| dc.contributor.thirdReferee | Heimel, Kai Prof. Dr. | |
| dc.contributor.thirdReferee | Ischebeck, Till Pd Dr. | |
| dc.subject.eng | Systemic acquired resistance | de |
| dc.subject.eng | Salicylic acid | de |
| dc.subject.eng | Plant-microbe interactions | de |
| dc.identifier.urn | urn:nbn:de:gbv:7-21.11130/00-1735-0000-0008-57CB-2-2 | |
| dc.affiliation.institute | Göttinger Graduiertenschule für Neurowissenschaften, Biophysik und molekulare Biowissenschaften (GGNB) | de |
| dc.subject.gokfull | Biologie (PPN619462639) | de |
| dc.identifier.ppn | 1752572513 | |