Autoimmunity conferred by chs3-2D relies on CSA1, its adjacent TIR-NB-LRR encoding neighbour

Plant innate immunity depends on the function of a large number of intracellular immune receptor proteins, the majority of which are structurally similar to mammalian nucleotidebinding oligomerization domain (NOD)-like receptor (NLR) proteins. CHILLING SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an additional Lin-11, Isl-1 and Mec-3 (LIM) domain at its C-terminus. The gain-of-function mutant allele chs3-2D exhibits severe dwarfism and constitutively activated defense responses, including enhanced resistance to virulent pathogens, high defence marker gene expression, and salicylic acid accumulation. To search for novel regulators involved in CHS3-mediated immune signaling, we conducted suppressor screens in the chs3-2D and chs3-2D pad4-1 genetic backgrounds. Alleles of sag101 and eds1-90 were isolated as complete suppressors of chs3-2D, and alleles of sgt1b were isolated as partial suppressors of chs3-2D pad4-1. These mutants suggest that SAG101, EDS1-90, and SGT1b are all positive regulators of CHS3-mediated defense signaling. Additionally, the TIR-type NLR-encoding CSA1 locus located genomically adjacent to CHS3 was found to be fully required for chs3-2D-mediated autoimmunity. CSA1 is located 3.9kb upstream of CHS3 and is transcribed in the opposite direction. Altogether, these data illustrate the distinct genetic requirements for CHS3-mediated defense signaling

The Protein Phosphatase 7 Regulates Phytochrome Signaling in Arabidopsis

The psi2 mutant of Arabidopsis displays amplification of the responses controlled by the red/far red light photoreceptors phytochrome A (phyA) and phytochrome B (phyB) but no apparent defect in blue light perception. We found that loss-of-function alleles of the protein phosphatase 7 (AtPP7) are responsible for the light hypersensitivity in psi2 demonstrating that AtPP7 controls the levels of phytochrome signaling. Plants expressing reduced levels of AtPP7 mRNA display reduced blue-light induced cryptochrome signaling but no noticeable deficiency in phytochrome signaling. Our genetic analysis suggests that phytochrome signaling is enhanced in the AtPP7 loss of function alleles, including in blue light, which masks the reduced cryptochrome signaling. AtPP7 has been found to interact both in yeast and in planta assays with nucleotide-diphosphate kinase 2 (NDPK2), a positive regulator of phytochrome signals. Analysis of ndpk2-psi2 double mutants suggests that NDPK2 plays a critical role in the AtPP7 regulation of the phytochrome pathway and identifies NDPK2 as an upstream element involved in the modulation of the salicylic acid (SA)-dependent defense pathway by light. Thus, cryptochrome- and phytochrome-specific light signals synchronously control their relative contribution to the regulation of plant development. Interestingly, PP7 and NDPK are also components of animal light signaling systems

A Constitutive Shade-Avoidance Mutant Implicates TIR-NBS-LRR Proteins in Arabidopsis Photomorphogenic Development

In plants, light signals caused by the presence of neighbors accelerate stem growth and flowering and induce a more erect position of the leaves, a developmental strategy known as shade-avoidance syndrome. In addition, mutations in the photoreceptors that mediate shade-avoidance responses enhance disease susceptibility in Arabidopsis thaliana. Here, we describe the Arabidopsis constitutive shade-avoidance1 (csa1) mutant, which shows a shade-avoidance phenotype in the absence of shade and enhanced growth of a bacterial pathogen. The csa1 mutant has a T-DNA inserted within the second exon of a Toll/Interleukin1 receptor–nucleotide binding site–leucine-rich repeat (TIR-NBS-LRR) gene, which leads to the production of a truncated mRNA. Arabidopsis plants transformed with the truncated TIR-NBS-LRR gene recapitulate the mutant phenotype, indicating that csa1 is a dominant-negative mutation that interferes with phytochrome signaling. TIR-NBS-LRR proteins have been implicated in defense responses in plants. RPS4, the closest homolog of CSA1, confers resistance to Pseudomonas syringae and complements the csa1 mutant phenotype, indicating that responses to pathogens and neighbors share core-signaling components in Arabidopsis. In Drosophila melanogaster and Caenorhabditis elegans, TIR domain proteins are implicated in both development and immunity. Thus, the dual role of the TIR domain is conserved across kingdoms

Autoimmunity conferred by chs3-2D relies on CSA1, its adjacent TNL-encoding neighbour

Plant innate immunity depends on the function of a large number of intracellular immune receptor proteins, the majority of which are structurally similar to mammalian nucleotidebinding oligomerization domain (NOD)-like receptor (NLR) proteins. CHILLING SENSITIVE 3 (CHS3) encodes an atypical Toll/Interleukin 1 Receptor (TIR)-type NLR protein with an additional Lin-11, Isl-1 and Mec-3 (LIM) domain at its C-terminus. The gain-of-function mutant allele chs3-2D exhibits severe dwarfism and constitutively activated defense responses, including enhanced resistance to virulent pathogens, high defence marker gene expression, and salicylic acid accumulation. To search for novel regulators involved in CHS3-mediated immune signaling, we conducted suppressor screens in the chs3-2D and chs3-2D pad4-1 genetic backgrounds. Alleles of sag101 and eds1-90 were isolated as complete suppressors of chs3-2D, and alleles of sgt1b were isolated as partial suppressors of chs3-2D pad4-1. These mutants suggest that SAG101, EDS1-90, and SGT1b are all positive regulators of CHS3-mediated defense signaling. Additionally, the TIR-type NLR-encoding CSA1 locus located genomically adjacent to CHS3 was found to be fully required for chs3-2D-mediated autoimmunity. CSA1 is located 3.9kb upstream of CHS3 and is transcribed in the opposite direction. Altogether, these data illustrate the distinct genetic requirements for CHS3-mediated defense signaling

Loss and retention of resistance genes in five species of the Brassicaceae family

Background: Plants have evolved disease resistance (R) genes encoding for nucleotide-binding site (NB) and leucine-rich repeat (LRR) proteins with N-terminals represented by either Toll/Interleukin-1 receptor (TIR) or coiled-coil (CC) domains. Here, a genome-wide study of presence and diversification of CC-NB-LRR and TIR-NB-LRR encoding genes, and shorter domain combinations in 19 Arabidopsis thaliana accessions and Arabidopsis lyrata, Capsella rubella, Brassica rapa and Eutrema salsugineum are presented.Results: Out of 528 R genes analyzed, 12 CC-NB-LRR and 17 TIR-NB-LRR genes were conserved among the 19 A. thaliana genotypes, while only two CC-NB-LRRs, including ZAR1, and three TIR-NB-LRRs were conserved when comparing the five species. The RESISTANCE TO LEPTOSPHAERIA MACULANS 1 (RLM1) locus confers resistance to the Brassica pathogen L. maculans the causal agent of blackleg disease and has undergone conservation and diversification events particularly in B. rapa. On the contrary, the RLM3 locus important in the immune response towards Botrytis cinerea and Alternaria spp. has recently evolved in the Arabidopsis genus.Conclusion: Our genome-wide analysis of the R gene repertoire revealed a large sequence variation in the 23 cruciferous genomes. The data provides further insights into evolutionary processes impacting this important gene family