Complete Genome Sequence of Ralstonia solanacearum WR-1, a Virulent Strain on Solanum lycopersicum.

Ralstonia solanacearum is a bacterial wilt pathogen of Solanum lycopersicum. Its pathogenicity is the result of coevolution during continuous interaction with its host plants under given biotic and abiotic environments. To elucidate clues for pathogenicity of our WR-1 strain, its genome sequence was analyzed.

Complete Genome Sequence of Ralstonia pseudosolanacearum Strain Sw698, Isolated from Solanum lycopersicum.

Ralstonia pseudosolanacearum is a member of the Ralstonia solanacearum species complex (RSSC), which is composed of three species and diverse subspecific groups. Some strains cause bacterial wilt in Solanum lycopersicum; others are beneficial for their hosts. Herein, we present the complete genome sequence of an RSSC strain, Sw698, beneficial for S. lycopersicum growth.

Complete Genome Sequence of Ralstonia solanacearum Strain Bs715, a Member of Biovar 4 and a Strong Pathogen of Bacterial Wilt on Solanum lycopersicum.

Ralstonia solanacearum is a notorious pathogen of bacterial wilt on Solanum lycopersicum. Most isolates from diseased tomato tissues are biovar 3, and their genomes are publicly available; however, information on biovar 4 strains is limited. Here, the complete genome sequence of R. solanacearum Bs715, a biovar 4 strain, is presented.

OsDWD1 E3 ligase-mediated OsNPR1 degradation suppresses basal defense in rice.

Many ubiquitin E3 ligases function in plant immunity. Here, we show that Oryza sativa (rice) DDB1 binding WD (OsDWD1) suppresses immune responses by targeting O. sativa non-expresser of pathogenesis-related gene 1 (OsNPR1) for degradation. Knock-down and overexpression experiments in rice plants showed that OsDWD1 is a negative regulator of the immune response and that OsNPR1 is a substrate of OsDWD1 and a substrate receptor of OsCRL4. After constructing the loss-of-function mutant OsDWD1R239A , we showed that the downregulation of OsNPR1 seen in rice lines overexpressing wild-type (WT) OsDWD1 (OsDWD1WT -ox) was compromised in OsDWD1R239A -ox lines, and that OsNPR1 upregulation enhanced resistance to pathogen infection, confirming that OsCRL4OsDWD1 regulates OsNPR1 protein levels. The enhanced disease resistance seen in OsDWD1 knock-down (OsDWD1-kd) lines contrasted with the reduced disease resistance in double knock-down (OsDWD1/OsNPR1-kd) lines, indicating that the enhanced disease resistance of OsDWD1-kd resulted from the accumulation of OsNPR1. Moreover, an in vivo heterologous protein degradation assay in Arabidopsis thaliana ddb1 mutants confirmed that the CUL4-based E3 ligase system can also influence OsNPR1 protein levels in Arabidopsis. Although OsNPR1 was degraded by the OsCRL4OsDWD1 -mediated ubiquitination system, the phosphodegron-motif-mutated NPR1 was partially degraded in the DWD1-ox protoplasts. This suggests that there might be another degradation process for OsNPR1. Taken together, these results indicate that OsDWD1 regulates OsNPR1 protein levels in rice to suppress the untimely activation of immune responses.

WRKY10 transcriptional regulatory cascades in rice are involved in basal defense and Xa1-mediated resistance.

WRKY proteins play essential roles as negative or positive regulators of pathogen defense. This study explored the roles of different OsWRKY proteins in basal defense and Xa1-mediated resistance to Xanthomonas oryzae pv. oryzae (Xoo) infection in rice. Assays of disease in OsWRKY10KD and OsWRKY88KD lines following infection with an incompatible Xoo race, which induced Xa1-mediated resistance in wild-type plants, showed that OsWRKY10 and OsWRKY88 were positive regulators of Xa1-mediated resistance. OsWRKY10 also acted as a positive regulator in basal defense by directly or indirectly activating transcription of defense-related genes. OsWRKY10 activated the OsPR1a promoter by binding to specific WRKY binding sites. Two transcriptional regulatory cascades of OsWRKY10 were identified in basal defense and Xa1-mediated resistance. In the first transcriptional regulatory cascade, OsWRKY47 acted downstream of OsWRKY10 whereas OsWRKY51 acted upstream. OsWRKY10 activated OsPR1a in two distinct ways: by binding to its promoter and, at the same time, by indirect activation through OsWRKY47. In the second transcriptional regulatory cascade, OsWRKY47 acted downstream of OsWRKY10, and OsWRKY88 acted upstream. These OsWRKY10 transcriptional regulatory cascades played important roles in basal defense and Xa1-mediated resistance to enable the mounting of a rapid immune response against pathogens.