Abstract

Systemic acquired resistance (SAR) is a plant immune response induced by local necrotizing pathogen infections. Expression of SAR in Arabidopsis (Arabidopsis thaliana) plants correlates with accumulation of salicylic acid (SA) and up-regulation of Pathogenesis-Related (PR) genes. SA is an essential and sufficient signal for SAR. In a genetic screen to search for negative regulators of PR gene expression and SAR, we found a new mutant that is hypersensitive to SA and exhibits enhanced induction of PR genes and resistance against the virulent oomycete Hyaloperonospora arabidopsidis Noco2. The enhanced pathogen resistance in the mutant is Nonexpressor of PR genes1 independent. The mutant gene was identified by map-based cloning, and it encodes a protein with high homology to Replication Factor C Subunit3 (RFC3) of yeast and other eukaryotes; thus, the mutant was named rfc3-1. rfc3-1 mutant plants are smaller than wild-type plants and have narrower leaves and petals. On the epidermis of true leaves, there are fewer cells in rfc3-1 compared with the wild type. Cell production rate is reduced in rfc3-1 mutant roots, indicating that the mutated RFC3 slows down cell proliferation. As Replication Factor C is involved in replication-coupled chromatin assembly, our data suggest that chromatin assembly and remodeling may play important roles in the negative control of PR gene expression and SAR.

Highlights

  • Systemic acquired resistance (SAR) is a plant immune response induced by local necrotizing pathogen infections

  • To identify additional negative regulators of PR gene expression and SAR, we screened for mutants that are hypersensitive to salicylic acid (SA) induction and found one with similar phenotypes to sni1

  • We searched for mutants showing strong GUS staining when grown on Murashige and Skoog (MS) plates supplemented with 10 mM SA

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Summary

Introduction

Systemic acquired resistance (SAR) is a plant immune response induced by local necrotizing pathogen infections. In 1961, Ross found that tobacco (Nicotiana tabacum) plants challenged with Tobacco mosaic virus subsequently developed enhanced resistance to secondary infections in distal tissues (Ross, 1961) This spread of resistance throughout the plant was termed systemic acquired resistance (SAR). When NPR1 is mutated, plants can no longer mount a SAR response even with induction of SA or INA (Cao et al, 1994). It functions through associations with TGA transcription factors to regulate PR gene expression and pathogen resistance (Durrant and Dong, 2004). A triple knockout mutant of TGA2, TGA5, and TGA6 displayed compromised SAR responses and increased basal PR gene expression, suggesting that TGA transcription factors have both positive and negative roles in regulating PR gene expression and SAR (Zhang et al, 2003)

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