Mutations in PMR5 result in powdery mildew resistance and altered cell wall composition
Powdery mildews and other obligate biotrophic pathogens are highly adapted to their hosts and often show
limited host ranges. One facet of such host specialization is likely to be penetration of the host cell wall, a major
barrier to infection. A mutation in the pmr5 gene rendered Arabidopsis resistant to the powdery mildew
species Erysiphe cichoracearum and Erysiphe orontii, but not to the unrelated pathogens Pseudomonas
syringae or Peronospora parasitica. PMR5 belongs to a large family of plant-specific genes of unknown
function. pmr5-mediated resistance did not require signaling through either the salicylic acid or jasmonic acid/
ethylene defense pathways, suggesting resistance in this mutant may be due either to the loss of a
susceptibility factor or to the activation of a novel form of defense. Based on Fourier transform infrared
analysis, the pmr5 cell walls were enriched in pectin and exhibited a reduced degree of pectin modification
relative to wild-type cell walls. In addition, the mutant had smaller cells, suggesting a defect in cell expansion.
A double mutant with pmr6 (defective in a glycosylphosphatidylinositol-anchored pectate lyase-like gene)
exhibited a strong increase in total uronic acid content and a more severe reduction in size, relative to the
single mutants, suggesting that the two genes affect pectin composition, either directly or indirectly, via
different mechanisms. These two mutants highlight the importance of the host cell wall in plant-microbe
interactions.
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BibTex references
@Article\{VRSS04, author = "Vogel, John P. and Raab, Theodore K. and Somerville, Chris R. and Somerville, Shauna C.", title = "Mutations in PMR5 result in powdery mildew resistance and altered cell wall composition", journal = "Plant Journal", volume = "40", pages = "968-978", year = "2004", note = "1.4.3", keywords = "Arabidopsis, cell wall, disease susceptibility, disease resistance, pectin, powdery mildew", url = "http://infrared.als.lbl.gov/Publications/2004/VRSS04" }