Structure-function analysis of npr1 alleles in Arabidopsis reveals a role for its paralogs in the perception of salicylic acid.

Plant Cell Environ

Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universidad Politécnica de Valencia (UPV)-Consejo Superior de Investigaciones Científicas (CSIC), Ciudad Politécnica de la Innovación (CPI), Ed. 8E C/ Ingeniero Fausto Elio s/n, 46022 Valencia, Spain.

Published: November 2010

AI Article Synopsis

  • Salicylic acid (SA) is crucial for plant defense against certain pathogens, while NPR1 is essential for perceiving SA and its analogues like benzothiadiazole (BTH) that enhance plant defense.
  • Mutants in Arabidopsis thaliana that cannot perceive BTH exhibit normal growth, allowing researchers to identify NPR1 allele mutants with similar characteristics in size and pathogen resistance.
  • The study finds that mutations are concentrated in the NPR1 protein and suggests the involvement of related NPR1 paralogs in SA signaling, particularly indicating their interaction with identified mutations that impair SA perception.

Article Abstract

Salicylic acid (SA) is necessary for plant defence against some pathogens, whereas NPR1 is necessary for SA perception. Plant defence can be induced to an extreme by several applications of benzothiadiazole (BTH), an analogue of SA. Thus, plants that do not perceive BTH grow unaffected, whereas wild-type plants grow stunted. This feature allows us to screen for mutants in Arabidopsis thaliana that show insensitivity to BTH in a high-throughput fashion. Most of the mutants are npr1 alleles, with similar phenotypes in plant weight and pathogen growth. The mutations are clustered in the carboxyl-terminal part of the protein, and no obvious null alleles were recovered. These facts have prompted a search for knockouts in the NPR1 gene. Two of these KO alleles identified are null and have an intermediate phenotype. All the evidence presented lead us to propose a redundancy in SA perception, with the paralogs of NPR1 taking part in this signalling. We show that the mutations recovered in the screening genetically interact with the paralogs preventing their function in SA signalling.

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Source
http://dx.doi.org/10.1111/j.1365-3040.2010.02194.xDOI Listing

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