English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Poster

Plant autoimmunity activated by oligomerization of the atypical resistance protein RPW8/HR4 and NLR RPP7

MPS-Authors
/persons/resource/persons272379

Li,  L
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons85266

Weigel,  D       
Department Molecular Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Li, L., & Weigel, D. (2019). Plant autoimmunity activated by oligomerization of the atypical resistance protein RPW8/HR4 and NLR RPP7. Poster presented at XVIII Congress of the International Society for Molecular Plant-Microbe Interactions (IS-MPMI 2019), Glasgow, UK.


Cite as: https://hdl.handle.net/21.11116/0000-000B-6C6A-6
Abstract
Immune responses that occur without an external trigger provide an effective platform for understanding the mechanisms underlying activation of immune signaling. In certain intra- and interspecific plant hybrids, autoimmunity can be triggered when immune system components meet that
have not been co-adapted. A particularly interesting case of hybrid necrosis in Arabidopsis thaliana is that of the RPP7 and RPW8 loci. RPP7, which confers race-specific resistance against oomycetes, encodes members of canonical coiled-coil, nucleotide-binding and leucine rich repeat
(CC-NLR) proteins. NLR proteins are the most common class of plant immune receptors. RPW8, which confers broad-spectrum resistance to biotrophic pathogens, belongs to the small family of RPW8/HR (Homologous to RPW8) coiled-coil-only domain proteins. Here, we will describe
the mechanisms by which the HR4Fei-0 and RPP7bLerik1-3 pair activates immune responses. Based on our findings, we propose a model that extends previous scenarios of NLR signaling based on ON/OFF equilibrium of closed, inactive and open, active NLR states.