The salicylic acid receptor NPR3 is a negative regulator of the transcriptional defense response during early flower development in Arabidopsis

Zi Shi, Siela Maximova, Yi Liu, Joseph Verica, Mark J. Guiltinan

Research output: Contribution to journalArticlepeer-review

42 Scopus citations

Abstract

Arabidopsis NON-EXPRESSOR OF PR1 (NPR1) is a transcription co-activator that plays a central role in regulating the transcriptional response to plant pathogens. The NPR family consists of NPR1 and five NPR1-like genes. The NPR1 paralog NPR3 has recently been shown to function as a receptor of the plant hormone salicylic acid and to mediate proteosomal degradation of NPR1. The function of NPR3 protein during early flower development was revealed through a detailed molecular-genetic analysis including promoter transcriptional fusion analysis, phenotype characterization of npr3-3 mutants/overexpressors, and whole-plant fitness analysis. The physical interaction between NPR3 and NPR1/TGA2 was explored using bimolecular fluorescence complementation analysis in onion epidermal cells. Here, we show that NPR3 expression was strongest in the petals and sepals of developing flowers and declined after flower opening. Consistently with this observation, an npr3 knockout mutant displayed enhanced resistance to Pseudomonas syringae infection of immature flowers, but not leaves. Developing npr3 flowers exhibited increased levels of basal and induced PR1 transcript accumulation. However, the npr3 mutant showed lower fitness compared to Col-0 in the absence of pathogen. Moreover, NPR3 was shown to interact with NPR1 and TGA2 in vivo. Our data suggest that NPR3 is a negative regulator of defense responses during early flower development and it may function through the association with both NPR1 and TGA2.

Original languageEnglish (US)
Pages (from-to)802-816
Number of pages15
JournalMolecular plant
Volume6
Issue number3
DOIs
StatePublished - May 2013

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Plant Science

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