Format

Send to

Choose Destination
See comment in PubMed Commons below
Plant Cell Environ. 2011 Nov;34(11):1944-57. doi: 10.1111/j.1365-3040.2011.02390.x. Epub 2011 Jul 25.

An Arabidopsis (malectin-like) leucine-rich repeat receptor-like kinase contributes to downy mildew disease.

Author information

1
Plant-Oomycete Interaction Group, UMR-Interactions Biotiques et Santé Végétale, INRA1301-CNRS6243-Université Nice-Sophia Antipolis, 06903, Sophia Antipolis, France.

Abstract

Biotrophic filamentous plant pathogens frequently establish intimate contact with host cells through intracellular feeding structures called haustoria. To form and maintain these structures, pathogens must avoid or suppress defence responses and reprogramme the host cell. We used Arabidopsis whole-genome microarrays to characterize genetic programmes that are deregulated during infection by the biotrophic' oomycete downy mildew pathogen, Hyaloperonospora arabidopsidis. Marked differences were observed between early and late stages of infection, but a gene encoding a putative leucine-rich repeat receptor-like kinase (LRR-RLK) was constantly up-regulated. We investigated the evolutionary history of this gene and noticed it being one of the first to have emerged from a common ancestral gene that gave rise to a cluster of 11 genes through duplications. The encoded LRR-RLKs harbour an extracellular malectin-like (ML) domain in addition to a short stretch of leucine-rich repeats, and are thus similar to proteins from the symbiosis receptor-like kinase family. Detailed expression analysis showed that the pathogen-responsive gene was locally expressed in cells surrounding the oomycete. A knockout mutant showed reduced downy mildew infection, but susceptibility was fully restored through complementation of the mutation, suggesting that the (ML-)LRR-RLK contributes to disease. According to the mutant phenotype, we denominated it Impaired Oomycete Susceptibility 1 (IOS1).

[Indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley
    Loading ...
    Support Center