Search

Grape white rot is a devastating fungal disease caused by Coniella diplodiella. The pathogen delivers effectors into the host cell that target crucial immune components to facilitate its infection. Here, we examined a secreted effector of C. diplodiella , known as CdE1, which has been found to inhibit Bax-triggered cell death in Nicotiana benthamiana plants. The expression of CdE1 was induced at 12–48 h after inoculation with C. diplodiella , and the transient overexpression of CdE1 led to increased susceptibility of grapevine to the fungus. Subsequent experiments revealed an interaction between CdE1 and Vitis davidii cysteine-rich receptor-like kinase 10 (VdCRK10) and suppression of VdCRK10-mediated immunity against C. diplodiella , partially by decreasing the accumulation of VdCRK10 protein. Furthermore, our investigation revealed that CRK10 expression was significantly higher and was up-regulated in the resistant wild grapevine V. davidii during C. diplodiella infection. The activity of the VdCRK10 promoter is induced by C. diplodiella and is higher than that of Vitis vitifera VvCRK10 , indicating the involvement of transcriptional regulation in CRK10 gene expression. Taken together, our results highlight the potential of VdCRK10 as a resistant gene for enhancing white rot resistance in grapevine. [ABSTRACT FROM AUTHOR]

Methyl jasmonate (MeJA) plays a vital role in plant disease resistance and also induces the expression of disease resistance genes in plants. In this study, a transcriptome analysis was performed on grapevine leaves after 12, 24 and 48 h of MeJA-100 μM treatment. A total of 1242 differentially expressed genes (DEGs) were identified from the transcriptome data, and the analysis of the DEGs showed that genes related to phytohormone signal transduction, jasmonic acid-mediated defense, Mitogen-activated protein kinase (MAPK), and flavonoid biosynthetic pathways were upregulated. As Pathogenesis-related gene 1 (PR1) is an important marker gene in plant defense also upregulated by MeJA treatment in RNA-seq data, the VvPR1 gene was selected for a promoter analysis with β-glucuronidase (GUS) through transient expression in tobacco leaves against abiotic stress. The results showed that the region from −1837 bp to −558 bp of the VvPR1 promoter is the key region in response to hormone and wound stress. In this study, we extended the available knowledge about induced defense by MeJA in a grapevine species that is susceptible to different diseases and identified the molecular mechanisms by which this defense might be mediated. [ABSTRACT FROM AUTHOR]

Grape white rot caused by Coniella diplodiella (Speg.) affects the production and quality of grapevine in China and other grapevine-growing countries. Despite the importance of C. diplodiella as a serious disease-causing agent in grape, the genome information and molecular mechanisms underlying its pathogenicity are poorly understood. To bridge this gap, 40.93 Mbp of C. diplodiella strain WR01 was de novo assembled. A total of 9,403 putative protein-coding genes were predicted. Among these, 608 and 248 genes are potentially secreted proteins and candidate effector proteins (CEPs), respectively. Additionally, the transcriptome of C. diplodiella was analyzed after feeding with crude grapevine leaf homogenates, which reveals the transcriptional expression of 9,115 genes. Gene ontology enrichment analysis indicated that the highly enriched genes are related with carbohydrate metabolism and secondary metabolite synthesis. Forty-three putative effectors were cloned from C. diplodiella , and applied for further functional analysis. Among them, one protein exhibited strong effect in the suppression of BCL2-associated X (BAX)-induced hypersensitive response after transiently expressed in Nicotiana benthamiana leaves. This work facilitates valuable genetic basis for understanding the molecular mechanism underlying C. diplodiella -grapevine interaction. [ABSTRACT FROM AUTHOR]

• Use the grape germplasm unique to China that is resistant to white rot disease, V. davidii Foex. 0941 as experimental materials. • By combining transcriptomic and metabolomic analyses, changes in genes and metabolites are studied in disease-resistant and disease-susceptible varieties after infection by fungus. • Analysis reveals that the flavonoid metabolic pathway plays a significant role in the disease resistance of V. davidii Foex. 0941. Grape white rot is a devastating disease caused by Coniella diplodiella (Speg.) Sacc. The wild Chinese grape variety Vitis davidii Foex. 0941 (V. davidii) exhibits strong resistance to this disease, which is crucial for the utilization of wild resources in developing new disease-resistant cultivars. However, the underlying mechanism of V. davidii' s resistance remains unclear. In this study, we collected berries from the disease-resistant V. davidii and the disease-susceptible Vitis vinifera 'Manicure Finger' (V. vinifera) after inoculation with the grape white rot fungus. Through transcriptome and metabolome analyses, we observed that in the berries of V. davidii , metabolites associated with flavonoid metabolism, including naringenin, tricetin, eriodictyol, luteolin, dihydrokaempferol, myricetin, and syringetin, are significantly enriched compared to those in V. vinifera. Moreover, core genes involved in flavonoid metabolism (F3′5′H, F3′H, PAL, FLS) are expressed at higher levels in V. davidii. We have also identified several candidate genes associated with flavonoids, including flavonoid 3′,5′-methyltransferase-like, cellulose synthase-like protein E6, and flavonoid 3′,5′-hydroxylase 2, which are highly expressed in V. davidii. This finding was further validated by qRT-PCR analysis, which also revealed higher expression levels of these genes in the resistant variety. Collectively, these results suggest that flavonoid compounds may play a key role in the resistance of V. davidii to Coniella diplodiella. [ABSTRACT FROM AUTHOR]