Project description:Larch (Larix spp.), a key species in China's reforestation efforts, faces increasing threats from shoot blight caused by Neofusicoccum laricinum. This study characterized the biological traits, virulence mechanisms, and host interactions of this pathogen to inform disease management. Twenty-five N. laricinum strains were isolated from six regions in Northeast China and identified through morphological and molecular analysis. Comprehensive growth assessments revealed optimal development at 18°C and pH 9-11, with significant strain-specific variation in virulence (lesions 18.4-38.8 mm). Pathogenicity assays revealed that the hypervirulent TM02 strain exhibited early and robust production of cell wall-degrading enzymes,such as pectin methylgalacturonase (PMG, 208.9 U/mg) and polygalacturonase (PG, 54.9 U/mg), correlated with its aggressive infection phenotype. Biochemical analyses revealed that the pathogen actively disrupted host oxidative defenses, with superoxide dismutase (SOD) activity peaking at 3 dpi (456.7 U/g·min-1) before decreasing to 0.8× control levels by 7 dpi, whereas peroxidase (POD) activity exhibited a transient 4.6-fold increase followed by rapid suppression. Transcriptome analysis revealed generally downregulation of defense genes, mainly cellulose synthase (21/25 genes) and peroxidase (38/45 genes), with –10.5-fold inhibition of Ces-g8671 and an –11.4-fold reduction in Pod-g18614 expression, indicating that pathogens can simultaneously damage larch cell wall synthesis and the ROS scavenging defense system. These findings establish N. laricinum’s sophisticated two-phase infection strategy: initial physical breach of cell walls facilitated by CWDEs, followed by systematic suppression of host antioxidant defenses. This study identifies specific molecular targets for developing intervention strategies and provides critical insights into host‒pathogen dynamics in larch plantations under climate change scenarios.
Project description:The bifunctional alkylating agent sulfur mustard (SM; bis-(2-dichloroethyl) sulfide) is a potent vesicating chemical that has previously been used as a chemical warfare agent. studies have shown that exposure to CWNA compounds induces damage in the brain and heart.
2016-08-30 | GSE54639 | GEO
Project description:Panax vietnamensis transcriptome after Neofusicoccum ribis treatment
Project description:We have looked at the transcriptional response of well characterised Synechococcus open ocean (WH8102) and coastal (CC9311) isolates to two DNA damaging agents, mitomycin C and ethidium bromide, using whole genome expression microarrays. The coastal strain, which was able to grow on higher concentrations of both chemicals, showed differential regulation of a larger proportion of its genome following M-bM-^@M-^Xtoxic shockM-bM-^@M-^Y treatment with each agent. Many of the orthologous genes in these strains, including those encoding sensor kinases, showed different transcriptional responses, with the CC9311 genes more likely to show significant changes for each tested treatment. While the overall response of each strain was considerably different, there were distinct transcriptional responses common to both strains observed for each DNA damaging agent, linked to the mode of action of each chemical. In both CC9311 and WH8102 there was evidence of SOS response induction under mitomycin C treatment, with genes encoding recA, the lexA repressor and umuC significantly upregulated in this experiment but not under ethidium bromide treatment. Conversely, ethidium bromide treatment tended to result in upregulation of the DNA-directed RNA polymerase genes, not observed following mitomycin C treatment. Interestingly, a large number of genes residing on putative genomic island regions of each genome also showed significant upregulation under one or both chemical treatments. In this series four conditions have been analyzed. These are 2 hour incubations (shock treatment) with ethidium bromide (EB, final conc 2ug/mL) and mitomycin C (MC, final conc 0.5 ug/mL) for Synechococcus sp. WH8102 and CC9311. For each slide, an experimental RNA sample was labeled with Cy3 or Cy5 and was hybridized with a reference RNA from a control sample (no addition of chemical agent) labeled with the other Cy dye. There are six slides per condition, each with at least two biological replicates and three technical replicates, including at least one flip-dye comparison. Each slide contains six replicate spots per gene.
Project description:We have looked at the transcriptional response of well characterised Synechococcus open ocean (WH8102) and coastal (CC9311) isolates to two DNA damaging agents, mitomycin C and ethidium bromide, using whole genome expression microarrays. The coastal strain, which was able to grow on higher concentrations of both chemicals, showed differential regulation of a larger proportion of its genome following ‘toxic shock’ treatment with each agent. Many of the orthologous genes in these strains, including those encoding sensor kinases, showed different transcriptional responses, with the CC9311 genes more likely to show significant changes for each tested treatment. While the overall response of each strain was considerably different, there were distinct transcriptional responses common to both strains observed for each DNA damaging agent, linked to the mode of action of each chemical. In both CC9311 and WH8102 there was evidence of SOS response induction under mitomycin C treatment, with genes encoding recA, the lexA repressor and umuC significantly upregulated in this experiment but not under ethidium bromide treatment. Conversely, ethidium bromide treatment tended to result in upregulation of the DNA-directed RNA polymerase genes, not observed following mitomycin C treatment. Interestingly, a large number of genes residing on putative genomic island regions of each genome also showed significant upregulation under one or both chemical treatments.