Gray mold disease caused by Botrytis cinerea is a devastating disease that leads to serious financial loss. In this study, the entomopathogenic fungus Metarhizium anisopliae that acts against the gray mold pathogen B. cinerea was evaluated. M. anisopliae produced a significant inhibition zone in front of the B. cinerea colony in the dual culture test. In addition, volatile organic compounds generated by M. anisopliae were shown to have an inhibitory effect on B. cinerea mycelia growth and reduced 41% of gray mold severity of postharvest tomatoes. The 10% concentration of the culture filtrate of M. anisopliae inhibited 88.62% of colony radial growth as well as 63.85% of sclerotia germination and all conidia germination of B. cinerea. Furthermore, the culture filtrate of M. anisopliae retained its inhibitory effect against the radial growth of B. cinerea even after heating for 15 min at 100 °C. Feasible mechanisms of M. anisopliae involved in the control of B. cinerea were explored, and it was demonstrated that the plasma membrane of B. cinerea conidia was damaged by the product of metabolism of M. anisopliae. In addition, after treating with culture filtrate of M. anisopliae, the B. cinerea phenotype was shown to be abnormal, and cell organelles of B. cinerea mycelia were damaged significantly. A significant control efficacy of M. anisopliae against tomato gray mold was detected on both the detached leaf assay (84.24%) as well as the whole plant (72.38%). In addition, a 78% reduction in tomato fruit mold was detected at a 10% treated concentration of M. anisopliae. These findings suggest that M. anisopliae possesses potential as a biocontrol agent against tomato gray mold in the greenhouse and during the postharvest stage.

Secreted effectors in plant root-knot nematodes (RKNs, or Meloidogyne spp.) play key roles in their parasite processes. Currently identified effectors mainly focus on the early stage of the nematode parasitism. There are only a few reports describing effectors that function in the latter stage. In this study, we identified a potential RKN effector gene, Misp12, that functioned during the latter stage of parasitism. Misp12 was unique in the Meloidogyne spp., and highly conserved in M. incognita. It encoded a secretory protein that specifically expressed in the dorsal esophageal gland, and highly up-regulated during the female stages. Transient expression of Misp12-GUS-GFP in onion epidermal cell showed that Misp12 was localized in cytoplast. In addition, in planta RNA interference targeting Misp12 suppressed the expression of Misp12 in nematodes and attenuated parasitic ability of M. incognita. Furthermore, up-regulation of Jasmonic acid (JA) and Salicylic acid (SA) pathway defense-related genes in the virus-induced silencing of Misp12 plants and down-regulation of SA pathway defense-related genes in Misp12-expressing plants indicated the gene might be associated with the suppression of the plant defense response. These results demonstrated that the novel nematode effector Misp12 played a critical role at latter parasitism of M. incognita.

Sclerotinia sclerotiorum is a cosmopolitan and typical necrotrophic phytopathogenic fungus that infects hundreds of plant species. Because no cultivars highly resistant to S. sclerotiorum are available, managing Sclerotinia disease caused by S. sclerotiorum is still challenging. However, recent studies have demonstrated that S. sclerotiorum has a beneficial effect and can live mutualistically as an endophyte in graminaceous plants, protecting the plants against major fungal diseases. An in‐depth understanding of the schizotrophic lifestyle of S. sclerotiorum during interactions with plants under different environmental conditions will provide new strategies for controlling fungal disease. In this review, we summarize the pathogenesis mechanisms of S. sclerotiorum during its attack of host plants as a destructive pathogen and discuss its lifestyle as a beneficial endophytic fungus.

Eggplant (Solanum melongena L.), which belongs to the Solanaceae family, is an important vegetable crop. However, its production is severely threatened by root-knot nematodes (RKNs) in many countries. Solanum torvum, a wild relative of eggplant, is employed worldwide as rootstock for eggplant cultivation due to its resistance to soil-borne diseases such as RKNs. In this study, to identify the RKN defense mechanisms, the transcriptomic profiles of eggplant and Solanum torvum were compared. A total of 5360 differentially expressed genes (DEGs) were identified for the response to RKN infection. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that these DEGs are mainly involved in the processes of response to stimulus, protein phosphorylation, hormone signal transduction, and plant-pathogen interaction pathways. Many phytohormone-related genes and transcription factors (MYB, WRKY, and NAC) were differentially expressed at the four time points (ck, 7, 14, and 28 days post-infection). The abscisic acid signaling pathway might be involved in plant-nematode interactions. qRT-PCR validated the expression levels of some of the DEGs in eggplant. These findings demonstrate the nematode-induced expression profiles and provide some insights into the nematode resistance mechanism in eggplant.

Understanding the reproduction and pathogenesis mechanism of phytopathogens could provide new opinions to effectively control fungal diseases. Although it has been known that effectors and extracellular hydrolytic enzymes secreted by phytopathogenic fungi play important roles in fungus-host interactions, the secretion system for the delivery of virulence factors to the host is still largely undescribed.

Summary: Plants are simultaneously attacked by different pests that rely on sugars uptake from plants. An understanding of the role of plant sugar allocation in these multipartite interactions is limited. Here, we characterized the expression patterns of sucrose transporter genes and evaluated the impact of targeted transporter gene mutants and brown planthopper (BPH) phloem‐feeding and oviposition on root sugar allocation and BPH‐reduced rice susceptibility to Meloidogyne graminicola. We found that the sugar transporter genes OsSUT1 and OsSUT2 are induced at BPH oviposition sites. OsSUT2 mutants showed a higher resistance to gravid BPH than to nymph BPH, and this was correlated with callose deposition, as reflected in a different effect on M. graminicola infection. BPH phloem‐feeding caused inhibition of callose deposition that was counteracted by BPH oviposition. Meanwhile, this pivotal role of sugar allocation in BPH‐reduced rice susceptibility to M. graminicola was validated on rice cultivar RHT harbouring BPH resistance genes Bph3 and Bph17. In conclusion, we demonstrated that rice susceptibility to M. graminicola is regulated by BPH phloem‐feeding and oviposition on rice through differences in plant sugar allocation.