Dataset Information

Proteome profiling of Cucurbita pepo phyllosphere after infection by Podosphaera xanthii and application of Reynoutria sachalinensis extract

ABSTRACT: Podosphaera xanthii is the main causal agent of powdery mildew (PM) disease for Cucurbita pepo. Disease control is attained principally by applications of chemical fungicides, along with parallel use of tolerant crop varieties and alternate application of elicitors to control development of disease resistance. To get insight into C. pepo molecular responses to P. xanthii infection and elicitor treatment we studied the proteomic profile differences at the phyllosphere of a zucchini cultivar susceptible to PM, at the onset of P. xanthii (PX) infection and after application of Reynoutria sachalinensis (RS) plant extract, respectively, using a nano-LC-HRMS/MS, Q-Exactive-Orbitrap approach. Analysis of peptide sequences regarding four treatment groups (Control; PX; RS; and RSPX (PX-infected priorly treated with RS)) resulted in 2070 CuGenDB annotations. Three comparisons (treatments vs Control) encompassed most of the Differentially Expressed Proteins (DEPs). In these three comparisons, KEGG and Gene Ontology functional analyses highlighted unique differentially enriched pathways -some of which including highly expressed proteins- in PX-related (Proteasome, Pentose phosphate pathway, and Carbon fixation), RS-related (Biosynthesis of Secondary metabolites, Flavonoids, and Starch and Sucrose metabolism), and RSPX-related (Pyruvate metabolism and Polycomb repressive complex) comparisons respectively, suggesting distinct mechanisms of early plant responses modulated by PX and RS. Furthermore, in four out of six comparisons the Thiamine metabolism pathway was found to be enriched, suggesting a pivotal role in PX-induced responses.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Cucurbita Pepo

TISSUE(S): Leaf

SUBMITTER: Ioannis Theologidis

LAB HEAD: Dimosthenis Kizis

PROVIDER: PXD057221 | Pride | 2024-11-07

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

Items per page:

1 - 5 of 19

Similar Datasets

Project description:Background - Multiple health effects are associated with moisture damage in buildings. Studies explaining these associations and cell-level mechanisms behind the observed health effects are urgently called for. Objectives - Alongside general toxicological markers, we focused on characterizing gene expression in human airway epithelium after exposure to indoor air particulate matter (PM) sampled from houses with and without moisture damage. Methods - We performed detailed technical building inspections in 25 residential houses and categorized them based on the detection of moisture damages and the probability of occupant exposure. PM sampling was complemented by microbiological and volatile organic compound assessment. We exposed airway constructs to three doses (1:16, 1:8, 1:4) of PM from moisture-damaged (index) and non-moisture-damaged (reference) houses. The RNA of exposed constructs was sequenced targeting toxicology -related genes. We did groupwise comparisons between index and reference houses and pairwise comparisons in matched index/reference houses. We analyzed general toxicological markers and imaged the constructs with electron microscopy. Results - In pairwise comparison, several genes were differentially expressed. Genes related to multiple toxicological pathways were highlighted, while none of the genes was consistently expressed in all the comparisons. In groupwise comparison, CYP1A1 was statistically significantly over-expressed in index houses at all doses (dose 1:16 log2FC = 0.007, padj = 0.03; dose 1:8 log2FC = 0.077, padj = 0.018; dose 1:4 log2FC = 0.270, padj = 0.002) and NFKB1 at the highest dose 1:4 (log2FC = 0.124, padj = 0.029). General toxicological markers did not separate the index/reference houses. Discussion - The exposure to PM from index houses activates toxicology -related genes in airway constructs. While differential expression was not consistent among all the index/reference pairs, possibly due to compositional differences of bioactive particles, our study highlights CYP1A1 and NFKB1 as potential targets in moisture damage -associated cellular responses.

Project description:Background: Pre-existing metabolic diseases may predispose individuals to particulate matter (PM)-induced adverse health effects. However, the differences in susceptibility of various metabolic diseases to PM-induced lung injury and their underlying mechanisms have yet to be fully elucidated. Results: Type 1 diabetes (T1D) or diet-induced obesity (DIO) murine models were generated by injection of streptozotocin or feeding a 45% high-fat diet for 10 weeks, respectively, and subjected to 4-week real-ambient PM exposure in Shijiazhuang, China (mean PM2.5 concentration 95.77 μg/m3). Pulmonary and systemic injury was assessed, and the underlying mechanisms were explored through transcriptomics analysis. Compared with normal diet (ND)-fed mice, T1D mice exhibited severe hyperglycemia with a blood glucose of 350 mg/dL, while DIO mice displayed moderate obesity and marked dyslipidemia with a slightly elevated blood glucose of 180 mg/dL. T1D and DIO mice were susceptible to PM-induced lung injury, manifested by inflammatory changes such as interstitial neutrophil infiltration and alveolar septal thickening. Notably, the acute lung injury scores were higher by 79.57% and 48.47%, respectively, than that of ND-fed mice. Lung transcriptome analysis revealed that increased susceptibility to PM exposure was associated with perturbations in multiple pathways including glucose and lipid metabolism, inflammatory responses, oxidative stress, cellular senescence, and tissue remodeling. Functional experiments confirmed that changes in biomarkers of macrophage (F4/80), lipid peroxidation (4-HNE), cellular senescence (SA-β-gal), and airway repair (CCSP) were most pronounced in the lungs of PM-exposed T1D mice. Furthermore, pathways associated with xenobiotic metabolism showed metabolic state- and tissue-specific perturbation patterns. Upon PM exposure, activation of nuclear receptor (NR) pathways and inhibition of the glutathione (GSH)-mediated detoxification pathway were evident in the lungs of T1D mice, and a significant upregulation of NR pathways was present in the livers of T1D mice. Conclusions: These differences might contribute to differential susceptibility to PM exposure between T1D and DIO mice. These findings provide new insights into the health risk assessment of PM exposure in populations with metabolic diseases.

			Action	DRS
	Control_1.raw	Raw
	Control_2.raw	Raw
	Control_3.raw	Raw
	Control_4.raw	Raw
	Cpepo_31_8_21.mzML	Mzml

Dataset Information

Proteome profiling of Cucurbita pepo phyllosphere after infection by Podosphaera xanthii and application of Reynoutria sachalinensis extract

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets