Search

Systemic acquired resistance (SAR) is a defense mechanism induced in the distal parts of plants after primary infection. It confers long-lasting protection against a broad spectrum of microbial pathogens. Lack of high-throughput assays has hampered the forward genetic analysis of SAR. Here, we report the development of an easy and efficient assay for SAR and its application in a forward genetic screen for SAR-deficient mutants in Arabidopsis (Arabidopsis thaliana). Using the new assay for SAR, we identified six flavin-dependent monooxygenasel, four AGD2-Iike defense response protein1, three salicylic acid induction-deficient2, one phytoalexin deficient4, and one avrPphB-susceptible3 alleles as well as a gain-of-function mutant of CALMODULIN-BINDING TRANSCRIPTION ACTIVATOR3 designated camta3-3D. Like transgenic plants overexpressing CAMTA3, camta3-3D mutant plants exhibit compromised SAR and enhanced susceptibility to virulent pathogens, suggesting that CAMTA3 is a critical regulator of both basal resistance and SAR. [ABSTRACT FROM AUTHOR]

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 genesi 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-TI compared with the wild type. Cell production rate is reduced in rfc3-TI 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. [ABSTRACT FROM AUTHOR]