TaCAP1 Interacts with TaLHCB1s and Positively Regulates Wheat Resistance Against Stripe Rust.

Actin filaments and their associated actin-binding proteins play key roles in plant innate immune signaling. CAP1, or cyclase-associated protein 1, is an important regulatory factor of the actin cytoskeleton-associated signaling network and was hypothesized here to be involved in resistance against wheat stripe rust because TaCAP1 expression was upregulated in response to Puccinia striiformis f. sp. tritici (Pst). Downregulation of TaCAP1 expression led to decreased resistance against Pst, in contrast to increased resistance upon TaCAP1 overexpressing, as demonstrated by the changes of phenotypes and hyphal growth. We found increased expression of pathogenesis-responsive or relative related genes and disease grade changed in TaCAP1 overexpressing plants. Our results also showed TaCAP1-regulated host resistance to Pst by inducing the production and accumulation of reactive oxygen species and mediating the salicylic acid signaling pathway. Additionally, TaCAP1 interacted with chlorophyll a/b-binding proteins TaLHCB1.3 and TaLHCB1.4, also known as the light-harvesting chlorophyll-protein complex II subunit B, which belong to the light-harvesting complex II protein family. Silencing of two TaLHCB1 genes showed higher susceptibility to Pst, which reduced wheat resistance against Pst. Therefore, the data presented herein further illuminate our understanding that TaCAP1 interacts with TaLHCB1s and functions as a positive regulator of wheat resistance against stripe rust.

The Improved Biocontrol Agent, F1-35, Protects Watermelon against Fusarium Wilt by Triggering Jasmonic Acid and Ethylene Pathways.

Watermelon Fusarium wilt, caused by Fusarium oxysporum f. sp. niveum (FON), is one of the most important diseases, and has become a major limiting factor to watermelon production worldwide. Previous research has found that the improved biocontrol agent, F1-35, had a high control efficiency to watermelon Fusarium wilt. In this study, the control efficiency of F1-35 to watermelon Fusarium wilt was firstly tested, and the control efficiency was 61.7%. Then, we investigated the mode of action of F1-35 in controlling watermelon Fusarium wilt. Using a pairing assay, we found that F1-35 did not inhibit the normal growth of FON. To know more about the interaction between F1-35 and watermelon root, the protein expressions of roots after 12, 24, and 48 h post-inoculation were examined. A total of 1109 differentially expressed proteins were obtained. KEGG analysis found that the most differentially expressed proteins occurred in alpha-linolenic acid metabolism, cysteine and methionine metabolism, plant-pathogen interaction, and the MAPK signaling pathway to the plant. A further analysis of differentially expressed proteins showed that F1-35 triggered the jasmonic acid and ethylene pathways in watermelon. To validate our results, the qRT-PCR was used to analyze the gene expression levels of PAL, LOX1, and CTR1. The gene expression results showed that those genes, which were positive correlated with the JA pathway, were up-expressed, including PAL and LOX1, and the negative associated gene, CTR1, was down-expressed. In conclusion, the improved biocontrol agent, F1-35, improves the resistance of watermelons to FON by triggering the JA and ET pathways.

Identification and Characterization of WRKY41, a Gene Conferring Resistance to Powdery Mildew in Wild Tomato (Solanum habrochaites) LA1777.

WRKYs, a large family of transcription factors, are involved in plant response to biotic and abiotic stresses, but the role of them in tomato resistance to Oidium neolycopersici is still unclear. In this study, we evaluate the role of WRKYs in powdery mildew-resistant wild tomato (Solanum habrochaites) LA1777 defense against O. neolycopersici strain lz (On-lz) using a combination of omics, classical plant pathology- and cell biology-based approaches. A total of 27 WRKYs, belonging to group I, II, and III, were identified as differentially expressed genes in LA1777 against On-lz. It was found that expression of ShWRKY41 was increased after Pseudomonas syringae pv. tomato (Pst) DC3000, On-lz and Botrytiscinerea B05 inoculation or ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) treatment. GUS staining of ShWRKY41 promoter indicated that the expression of ShWRKY41 could be induced by SA and ethylene. Furthermore, ShWRKY41 gene silencing reduced the resistance to On-lz infection by decreasing the generation of H2O2 and HR in LA1777 seedlings. Overall, our research suggests that ShWRKY41 plays a positive role in defense activation and host resistance to O. neolycopersici in wild tomato (S. habrochaites) LA1777.

ShNPSN11, a vesicle-transport-related gene, confers disease resistance in tomato to Oidium neolycopersici.

Tomato powdery mildew, caused by Oidium neolycopersici, is a fungal disease that results in severe yield loss in infected plants. Herein, we describe the function of a class of proteins, soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), which play a role in vesicle transport during defense signaling. To date, there have been no reports describing the function of tomato SNAREs during resistance signaling to powdery mildew. Using a combination of classical plant pathology-, genetics-, and cell biology-based approaches, we evaluate the role of ShNPSN11 in resistance to the powdery mildew pathogen O. neolycopersici. Quantitative RT-PCR analysis of tomato SNAREs revealed that ShNPSN11 mRNA accumulation in disease-resistant varieties was significantly increased following pathogen, compared with susceptible varieties, suggesting a role during induced defense signaling. Using in planta subcellular localization, we demonstrate that ShNPSN11 was primarily localized at the plasma membrane, consistent with the localization of SNARE proteins and their role in defense signaling and trafficking. Silencing of ShNPSN11 resulted in increased susceptibility to O. neolycopersici, with pathogen-induced levels of H2O2 and cell death elicitation in ShNPSN11-silenced lines showing a marked reduction. Transient expression of ShNPSN11 did not result in the induction of a hypersensitive cell death response or suppress cell death induced by BAX. Taken together, these data demonstrate that ShNPSNl11 plays an important role in defense activation and host resistance to O. neolycopersici in tomato LA1777.

The Biocontrol Efficacy of Streptomyces pratensis LMM15 on Botrytis cinerea in Tomato.

LMM15, an actinomycete with broad spectrum antifungal activity, was isolated from a diseased tomato leaf using the baiting technique. A phylogenetic tree analysis based on similarity percentage of 16S rDNA sequences showed that the bacterium was 97.0% affiliated with the species Streptomyces pratensis. This strain was therefore coded as S. pratensis LMM15. The ferment filtrate of LMM15 had ability to inhibit mycelia growth of Botrytis cinerea and reduce lesion expansion of gray mold on detached leaves and fruits. In greenhouse experiments, both the fresh and dry weights of tomato seedlings were significantly increased with the increased concentrations of total chlorophyll. The incidence of tomato gray mold decreased by 46.35%; this was associated with the increase of proline content and malondialdehyde (MDA) and the changes in defense-related enzymes on tomato leaves when the strain was sprayed on the tomato leaves 24 h prior to inoculation with pathogens. This study showed that the strain S. pratensis LMM15 could be a potential agent for controlling tomato gray mold.