Key metabolic, signalling and gene expression features in the selected hybrid that may be relevant for resistance are identified, including rapid triacylglycerols degradation, galactolipid peroxidation, constitutive higher SA level and expression of the defensin VviAMP1.
Abstract
Powdery mildew, caused by the obligate biotroph
Erysiphe necator
, represents a major threat to grapevine production worldwide. Host-mediated resistance offers a sustainable alternative to chemical fungicides. To elucidate the role of plant membrane lipid modifications and oxylipin accumulation in pathogen perception and response, a controlled infection experiment was conducted comparing a resistant hybrid (NY_39) from the Edmund Mach Foundation germplasm collection with a susceptible variety (cv. ‘Teroldego’).
A lipidomic approach was integrated with hormone profiling and lipoxygenase (LOX) gene expression analysis. Significant lipid modulation was observed following
E. necator
inoculation, highlighting the plasticity of membrane and storage lipids metabolism. A rapid decrease in triacylglycerol content was measured in NY_39 at 12 h post-inoculation (hpi), whereas the opposite trend occurred in ‘Teroldego’, suggesting divergent metabolic rearrangements. A fast galactolipids peroxidation occurred in NY_39, while a delayed accumulation of phosphatidic acid was observed in ‘Teroldego’ at 48 hpi. The resistant genotype exhibited higher constitutive levels of salicylic acid as well as the expression of the
VviAMP1
defensin, a small cysteine-rich protein with broad-spectrum antifungal activity.
VviPR10-s11
and
VviWRKY51
, related to the synthesis of lignin and stilbenoid phytoalexins, were induced at 12 hpi in both genotypes. Within the LOX family, significant up-regulation of the 9-LOX
VviLOX1a
and the 13-LOXs
VviLOX9
and
VviLOXO
was specific to ‘Teroldego’ at 12 hpi, despite a higher constitutive level of
VviLOX9
in NY_39.
This work identifies key metabolic, signalling and gene expression features in the selected hybrid that may be relevant for resistance. These include rapid triacylglycerols degradation, galactolipid peroxidation, constitutive higher SA level and expression of the defensin
VviAMP1
.
This multi-omics framework provides detailed lipidomic and transcriptomic signatures to identify candidate genes and lipid biomarkers for marker-assisted breeding of bacterial wilt-resistant peanut varieties.
Yu-Zhuo Xia, Zhenzhen Zhang, Jian Yang et al.· Agronomy· 0 citations
This study links major defense transcriptional programs and phytohormone dynamics, providing a comprehensive view of sugar beet responses to CLS, and revealed that a susceptible sugar beet genotype mounts an early and transient defense response against C. beticola.
Leonard Barnabas Ebinezer, Mari Natwick, Lorena I. Rangel et al.· BMC Plant Biology· 0 citations
Barley (Hordeum vulgare), a major cereal crop, suffers significant yield losses due to pathogen attack. Understanding the chemical defense responses that follow pathogen infection is essential to uncover new resistance targets in barley. In this study, we employed an untargeted metabolomics and mass spectrometry imaging approach to profile the chemical landscape of barley leaves inoculated with the hemibiotrophic fungal pathogen Pyrenophora teres f. teres, the causal agent of net blotch. Pathogen infection triggered a significant chemical defense response, including the induction of many phenylpropanoids and alkaloids. Specifically, a strong induction of tryptophan-derived metabolites was observed, including tryptamine, serotonin, and the novel 2-oxo-tryptamine (2OT), which accumulated at infection sites. Integration of transcriptomic-driven pathway discovery with biochemical characterization identified a flavin-containing monooxygenase (FMO) and a cytochrome P450 (CYP71P10) involved in 2OT and serotonin biosynthesis, respectively. Our results show increased metabolic investment toward indolic compounds in barley leaves following infection and activation of these pathways across different pathogens and cultivars suggests a conserved resistance mechanism. This study provides new insights into the barley defense response, offering new metabolic targets for the development of disease-resistant cereal crops.
Joachim Møller Christensen, Mette Marie Toldam-Andersen, H. J. L. Jørgensen et al.· Plant Physiology· 1 citation
White rot, caused by the Coniella diplodiella (Cd), is a devastating disease of grapevine that drives severe losses in yield and quality worldwide. NAC transcription factors are important regulators of plant immune responses. However, the functional roles and regulatory mechanisms of NAC in grapevine defense against Cd remain largely unclear. Here, we demonstrated that VlNAC29 acts as a key positive regulator of grapevine white rot resistance. We showed that NAC29 expression is significantly induced by the chitin, salicylic acid (SA), and Cd infection in both the white rot-resistant grape cultivar ('Zhuosexiang') and susceptible cultivars ('Thompson Seedless' or 'Red Globe'). Subcellular localization and transcriptional activity assays confirmed that VlNAC29 encodes a nuclear-localized protein with transactivation activity. Promoter reporter assays further revealed that the VlNAC29 promoter is strongly activated by SA and chitin. The overexpression of VlNAC29 in grapevine significantly enhanced resistance to Cd infection, as evidenced by enhancing antioxidant enzyme activity and markedly upregulating the expression of defense related genes. Integrative analysis of RNA-seq and qRT-PCR revealed that VlNAC29 modulates the expression of core genes involved in PTI, SA-mediated resistant pathway, and ROS metabolism. Collectively, our findings reveal that VlNAC29 orchestrates SA mediated defense and ROS homeostasis to enhance grapevine resistance against white rot. This research not only advances the mechanistic understanding of NAC mediated grapevine resistance response, but also provides a promising genetic target for molecular breeding of disease resistant grapevines.
Xiaoli Zhang, Yanqiu Du, Xiangyu Zhou et al.· Plant Science· 0 citations