Loss of a callose synthase results in salicylic acid-dependent disease resistance

Science. 2003 Aug 15;301(5635):969-72. doi: 10.1126/science.1086716.

Abstract

Plants attacked by pathogens rapidly deposit callose, a beta-1,3-glucan, at wound sites. Traditionally, this deposition is thought to reinforce the cell wall and is regarded as a defense response. Surprisingly, here we found that powdery mildew resistant 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more susceptible. This resistance was due to mutation of a callose synthase, resulting in a loss of the induced callose response. Double-mutant analysis indicated that blocking the salicylic acid (SA) defense signaling pathway was sufficient to restore susceptibility to pmr4 mutants. Thus, callose or callose synthase negatively regulates the SA pathway.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alleles
  • Arabidopsis / cytology
  • Arabidopsis / genetics
  • Arabidopsis / metabolism*
  • Arabidopsis / microbiology*
  • Ascomycota / physiology*
  • Cell Death
  • Gene Expression Profiling
  • Gene Expression Regulation, Plant
  • Genes, Plant
  • Glucans / metabolism
  • Glucosyltransferases / genetics*
  • Glucosyltransferases / metabolism
  • Membrane Proteins*
  • Mutation
  • Oligonucleotide Array Sequence Analysis
  • Phenotype
  • Plant Diseases*
  • Plant Leaves / metabolism
  • Salicylic Acid / metabolism*
  • Schizosaccharomyces pombe Proteins*
  • Signal Transduction

Substances

  • Glucans
  • Membrane Proteins
  • Schizosaccharomyces pombe Proteins
  • callose
  • Glucosyltransferases
  • 1,3-beta-glucan synthase
  • Salicylic Acid