Function and Regulation of Arabidopsis thaliana Helper NLRs during (Auto-) Immunity

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dc.contributor.advisor El Kasmi, Farid (Dr.) Saile, Svenja Corina 2022-05-06T10:40:11Z 2022-05-06T10:40:11Z 2024-03-28
dc.identifier.uri de_DE
dc.description.abstract Plants use a complex receptor-based immune system to resist pathogen attacks. Intracellular NUCLEOTIDE-BINDING LEUCINE-RICH REPEAT (NLR) proteins recognize pathogen-derived effector molecules to induce defense responses. Toll/interleukin-1 receptor resistance (TIR) domain-containing NLRs (TNLs) and coiled-coil (CC) domain-containing NLRs (CNLs) are the two major types of NLRs involved in effector recognition, and are therefore classified as sensor NLRs. Several CNLs and all tested TNLs require the presence of a third, evolutionary conserved family of NLRs, the RNL class, that is characterized by a N-terminal RESISTANCE TO POWDERY MILDEW 8 (RPW8)-like CC domain (CCR). The RNL family is formed by two subfamilies, ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1). While members of both RNL subfamilies are known to act downstream of multiple sensor NLRs in Arabidopsis thaliana, the specific and redundant functions of ADR1s and NRG1s are largely unknown. We demonstrated that ADR1s and NRG1s act mainly as unequal redundant nodes during basal resistance and sensor NLR-mediated immunity, albeit they also have distinct specificity towards certain sensor NLRs. Additionally, we showed that RNLs mediate TNL-triggered transcriptional changes that are similar to transcriptional changes induced by CNLs. Therefore, we propose that RNLs function similarly to CNLs to mediate defense responses downstream of all TNLs and some CNLs. Our analyses revealed that ADR1s can homo- and heterodimerize and that members of the ADR1 and NRG1 subfamilies require plasma membrane (PM) localization to function. This is consistent with other findings, indicating that RNL-independent CNLs also function at the PM. Remarkably, we also demonstrated that RNLs and the RNL-independent CNL Resistance to Pseudomonas syringae pv. maculicola 1 (RPM1) use a potentially conserved mechanism to localize to the PM by directly binding to PM-localized, negatively charged phospholipids. The PM localization of RNLs suggests that they could interact with other PM-localized proteins, important for plant immunity. In fact, we could show that members of the ADR1 subfamily interact with receptor kinases essential for PATTERN RECOGNITION RECEPTOR (PRR)-mediated immune responses. These results suggested that ADR1s might be involved in PRR-mediated immunity and/or that proteins associated with PRR-mediated immunity could also be required for helper NLR-mediated immune responses. We could indeed demonstrate that ADR1 family members play a critical role in PRR RECEPTOR-LIKE PROTEIN 23 (RLP23)-mediated immunity. Further, we have identified the PRR co-receptor protein BAK1-LIKE 1 (BKK1) as an essential factor for the autoimmune phenotype induced by the expression of the autoactivated ADR1-LIKE 2 (ADR1-L2D484V). Based on these findings we conclude that there is a mutual relationship between PRR- and NLR-mediated signaling that converges on the ADR1 node. Overall, the work reported in this PhD thesis provides new insights into RNL function and regulation and opens new avenues to study the interconnection of the two receptor-based plant immune branches – PRR- and NLR-mediated immunity. en
dc.description.abstract Dissertation ist gesperrt bis zum 28.03.2024 !! de_DE
dc.language.iso en de_DE
dc.publisher Universität Tübingen de_DE
dc.rights ubt-podok de_DE
dc.rights.uri de_DE
dc.rights.uri en
dc.subject.ddc 000 de_DE
dc.subject.ddc 500 de_DE
dc.subject.ddc 570 de_DE
dc.subject.other Pflanzliches Immunsystem de_DE
dc.subject.other ETI en
dc.subject.other ETI de_DE
dc.subject.other PTI de_DE
dc.subject.other PTI en
dc.subject.other Helfer NLRs de_DE
dc.subject.other Helper NLRs en
dc.subject.other Plant Immunity en
dc.title Function and Regulation of Arabidopsis thaliana Helper NLRs during (Auto-) Immunity en
dc.type Dissertation de_DE
dcterms.dateAccepted 2022-03-29
utue.publikation.fachbereich Biologie de_DE
utue.publikation.fakultaet 7 Mathematisch-Naturwissenschaftliche Fakultät de_DE
utue.publikation.noppn yes de_DE


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