Preexisting systemic acquired resistance suppresses hypersensitive response-associated cell death in Arabidopsis hrl1 mutant

Sendil K. Devadas, Ramesh Raina

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

The hypersensitive response (HR) displayed by resistant plants against invading pathogens is a prominent feature of plant-pathogen interactions. The Arabidopsis hypersensitive response like lesions1 (hrl1) mutant is characterized by heightened defense responses that make it more resistant to virulent pathogens. However, hrl1 suppresses avirulent pathogen-induced HR cell death. Furthermore, the high PR-1 expression observed in hrl1 remains unaltered after avirulent and virulent pathogen infections. The suppressed HR phenotype in hrl1 is observed even when an elicitor is expressed endogenously from an inducible promoter, suggesting that an impaired transfer of avirulent factors is not the reason. Interestingly, the lack of HR phenotype in hrl1 is reversed if the constitutive defense responses are compromised either by a mutation in NON EXPRESSOR OF PR-1 (NPR1) or by depleting salicylic acid due to the expression of the nahG gene. The rescue of HR cell death in hrl1 npr1 and in hrl1 nahG depends on the extent to which the constitutive systemic acquired response (SAR) is compromised. Pretreating Arabidopsis wild-type plants with SAR-inducers, before pathogen infection resulted in a significant decrease in HR cell death. Together, these results demonstrate that the preexisting SAR may serve as one form of negative feedback loop to regulate HR-associated cell death in hrl1 mutant and in the wild-type plants.

Original languageEnglish (US)
Pages (from-to)1234-1244
Number of pages11
JournalPlant Physiology
Volume128
Issue number4
DOIs
StatePublished - 2002

ASJC Scopus subject areas

  • Physiology
  • Genetics
  • Plant Science

Fingerprint Dive into the research topics of 'Preexisting systemic acquired resistance suppresses hypersensitive response-associated cell death in Arabidopsis hrl1 mutant'. Together they form a unique fingerprint.

  • Cite this