Dataset Information

Proteomic analysis of leucine effect on OMM protein turnover in C. elegans (Leu_CHX)

ABSTRACT: This project is to investigate whether and how leucine affects endogenous OMM protein stability in C. elegans. Whole worm and enriched mitochondria samples (with/without leucine and/or CHX treatment) were measured.

INSTRUMENT(S):

ORGANISM(S): Caenorhabditis Elegans

TISSUE(S): Whole Body

SUBMITTER: Prerana Wagle

LAB HEAD: Thorsten Hoppe

PROVIDER: PXD051401 | Pride | 2025-11-05

REPOSITORIES: Pride

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			Action	DRS
	20230915_E3_ColID_612_3562_01.raw	Raw
	20230915_E3_ColID_612_3562_02.raw	Raw
	20230915_E3_ColID_612_3562_03.raw	Raw
	20230915_E3_ColID_612_3562_04.raw	Raw
	20230915_E3_ColID_612_3562_05.raw	Raw

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Project description:Parental exposure to environmental stress can result in an increased diseases risk in the offspring. Although literature on maternal contribution to hereditary diseases are growing, the paternal contribution is frequently underrecognized. Since human studies reported that 80% of transmitted mutations arise in the paternal germline, it is crucial to understand the mechanism underlying the paternally inherited genome instability. Ionizing radiation (IR) is a major source of mutagenesis through inducing DNA double-strand breaks (DSBs). Here, we used sex-separated C. elegans mutants to investigate the paternal contribution to IR-induced transgenerational effects. Specifically, we found that paternal exposure to IR leads to a transgenerational embryonic lethality, and this effect is only observed when the radiation exposure occurred close to the time of fertilization. In the offspring of the irradiated males (F1 generation), we detected various genome instability phenotypes, including DNA fragmentation, chromosomal rearrangement, and aneuploidy. These phenotypes are attributed to the usage of two error-prone repair machinery, the polymerase-theta mediated end joining (TMEJ) and the non-homologous End Joining (NHEJ). Surprisingly, depletion of a human histone H1.0 ortholog, HIS-24, can significantly rescue this transgenerational embryonic lethality. Moreover, this rescue effect is associated with the downregulation of heterochromatin marker histone 3 lysine 9 di-methylation (H3K9me2), and the knocking-down of heterochromatin protein, HPL-1, could mimic the rescue effect of HIS-24 depletion. We also noticed that removal of the histone H1 and heterochromatin marker could activate the error-free repair machinery, Homologous Recombination repair (HR), thus improving the viability of the offspring carrying paternally inherited DNA damage. Altogether, our work sheds light on the importance of paternal radiation exposure on the health of offspring. In addition, our work establishes a previously unknown mechanism underlying the transgenerational genome instability and provides a potential therapeutic target for preventing the hereditary diseases caused by paternal radiation exposure.

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Proteomic analysis of leucine effect on OMM protein turnover in C. elegans (Leu_CHX)

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