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Chronic ionizing radiation suppresses resistance to pathogens in aquatic plants without substantial oxidative stress

ABSTRACT: Chronic ionizing radiation imposes direct and indirect damage on plants that could modify their morphology, biochemistry, physiology, as well as responses to biotic agents. Plants experience elevated levels of DNA damage and reactive oxygen species; thus, they adjust cellular homeostasis. Aquatic ecosystems in Chornobyl zone, a major radiological disaster site, are contaminated by harmful radionuclides. This study focused on changes in the proteome of leaves as well as carbonylated proteins, which might explain the biochemical mechanisms responsible for the susceptibility of a wild aquatic plant (common reed, Phragmites australis) grown in Chornobyl zone to biotic stress. The fungal infection assay indicated that life in a radionuclide-contaminated environment compromised plant immunity. The protein profiling identified 1,867 proteins; among them, 174 were differentially accumulated. We selected several dozen proteins with consistently higher and lower abundance in the samples from areas around the contaminated lakes by hierarchical clustering. Discordant expression of coding genes pointed to posttranscriptional regulation. Furthermore, the quantification of antioxidant enzyme activities (glutathione reductase, ascorbate peroxidase, catalase, and glutathione S-transferase) and carbonylated proteins rebutted the idea about substantial oxidative stress in chronically irradiated plants. We advocate the necessity to consider plausibly increased pathogen sensitivity while developing policies for the management of radionuclide-contaminated areas.

INSTRUMENT(S):

ORGANISM(S): Phragmites Australis

TISSUE(S): Plant Cell, Leaf

SUBMITTER: Maksym Danchenko

LAB HEAD: Peter Baráth

PROVIDER: PXD060551 | Pride | 2025-05-07

REPOSITORIES: Pride

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			Action	DRS
	20240419_ReedCarb_C1P1-C1P2_-40.mzXML	Mzxml
	20240419_ReedCarb_C1P1-C1P2_-60.mzXML	Mzxml
	20240419_ReedCarb_C1P1a_-40.mzXML	Mzxml
	20240419_ReedCarb_C1P1a_-60.mzXML	Mzxml
	20240419_ReedCarb_C1P2_-40.mzXML	Mzxml

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Project description:Exposure to Paraquat and RNA interference knockdown of mitochondrial superoxide dismutase (Sod2) are known to result in significant lifespan reduction, locomotor dysfunction, and mitochondrial degeneration in Drosophila melanogaster. Both perturbations increase the flux of superoxide, a progenitor reactive oxygen species, but the molecular underpinnings of the resulting phenotypes are poorly understood. Improved understanding of such processes could lead to advances in the treatment of numerous age-related disorders. Superoxide toxicity can act through protein carbonylation. Analysis of carbonylated proteins is attractive since reactive carbonyl groups are not present in the twenty canonical amino acids and are amenable to labeling and enrichment strategies. Here, carbonylated proteins were labeled with biotin hydrazide and enriched on streptavidin-coated beads. On-bead digestion was used to release carbonylated protein peptides, with relative abundance ratios versus controls obtained using the iTRAQ mass spectrometry-based proteomics approach. While Paraquat exposure and Sod2 knockdown have similar phenotypes, differences in protein carbonylation were anticipated because Paraquat exposure was expected to increase the concentration of superoxide throughout the cell while Sod2 knockdown was only expected to raise the concentration of superoxide in the mitochondrial matrix. Paraquat exposure resulted in widespread increases in carbonylated protein relative abundance: the median Paraquat-exposed to control carbonylated protein relative abundance ratio was 1.53. For Sod2 knockdown, in contrast, the median carbonylated protein relative abundance ratios were 1.13 versus the RNA interference driver control and 1.05 versus the RNA interference transgene control. However, some proteins did show large increases in carbonylated protein relative abundance on Sod2 knockdown, most notably cytochrome c oxidase subunit Vb, possibly providing some indication of the molecular basis of the Sod2-knockdown phenotype.

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Chronic ionizing radiation suppresses resistance to pathogens in aquatic plants without substantial oxidative stress

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