Abstract
In Nicotiana benthamiana, expression of the Xanthomonas effector XopQ triggers ROQ1-dependent ETI responses and in parallel accumulation of plastids around the nucleus and the formation of stromules. Both processes were proposed to contribute to ETI-related hypersensitive cell death and thereby to plant immunity. Whether these reactions are directly connected to ETI signaling events has not been tested. Here we utilized transient expression experiments to determine whether XopQ-mediated plastid reactions are a result of XopQ perception by ROQ1 or a consequence of XopQ virulence activity. We find that N. benthamiana mutants lacking ROQ1, both RNLs (NRG1 and ADR1) or EDS1, fail to elicit XopQ-dependent host cell death and stromule formation. Mutants lacking only NRG1 lost XopQ-dependent cell death but retained some stromule induction that was abolished in the RNL double mutant. This analysis aligns XopQ-induced stromules with the ETI signaling cascade but not to host programmed cell death. Furthermore, data reveal that XopQ-triggered plastid clustering is not strictly linked to stromule formation during ETI. Our data suggest that stromule formation, in contrast to chloroplast peri-nuclear dynamics, is an integral part of the N. benthamiana ETI response and that both RNL sub-types play a role in this ETI response.
One sentence summary Genetic analysis aligns effector triggered immunity (ETI) induced stromule formation with the ETI signaling cascade but not programmed cell death and questions stromule guided peri-nuclear plastid clustering.
Footnotes
Author for contact: Martin Hartmut Schattat, martin.schattat{at}pflanzenphys.uni-halle.de, +49 345 55 26286
The authors responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is Martin Hartmut Schattat (martin.schattat{at}pflanzenphys.uni-halle.de), Jane Parker (parker{at}mpipz.mpg.de) and Johannes Stuttmann (jstuttmann{at}gmail.com).
This study was funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – 400681449/GRK2498, STU642/1-1 and SFB-1403–414786233 as well as Martin-Luther-University core funding.