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Proteomic profiling of UV damage repair patches

ABSTRACT: DNA damage compromises not only genome stability but also the integrity of the chromatin template, which plays a central role in controlling cell identity. Our understanding of chromatin repair mechanisms is very incomplete. To bridge this knowledge gap, here we devised a novel proteomic strategy to characterize dynamic changes in the chromatin landscape during the repair of UV-induced DNA lesions in human cells, in a quantitative, unbiased and time-resolved manner. Based on the established IPOND methodology (Isolation of Proteins On Nascent DNA), we called this method IPOND-R for Isolation of Proteins On Nascent DNA at Repair sites.

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ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Yohann Couté

LAB HEAD: Yohann Couté

PROVIDER: PXD055129 | Pride | 2026-01-12

REPOSITORIES: Pride

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Project description:Radiation is an established cause of thyroid cancer and growing evidence supports a role for H2O2 in spontaneous thyroid carcinogenesis. Little is known about the molecular programs activated by these agents in thyroid cells. We profiled the DNA damage response and cell death induced by M-NM-3-radiation (0.1M-bM-^@M-^S5Gy) and H2O2 (0.0025M-bM-^@M-^S0.3mM) in primary human thyroid cells and T-cells. While the two cell types had more comparable radiation responses, 3- to 10-fold more H2O2 was needed to induce detectable DNA damage in thyrocytes. At H2O2 and radiation doses incurring double-strand breaks (DSB), cell death occurred after 24hrs in T-cells, but not in thyrocytes. We next prepared thyroid and T-cells primary cultures from 8 donors operated for non-cancerous pathologies and profiled their genome-wide transcriptional response 4hr after: 1) exposure to 1 Gy radiation, 2) treatment with H2O2, or 3) no treatment. Two H2O2 doses were investigated, calibrated in each cell type as to elicit levels of single- and double-strand breaks equivalent to 1 Gy M-NM-3-radiation. The transcriptional responses of thyrocyte and T-cells to radiation were similar, involving DNA repair and cell death genes. In addition to this transcriptional program, H2O2 also upregulated antioxidant genes in thyrocytes, including glutathione peroxidases (GPx) at the DSB-inducing dose. By contrast, a transcriptional storm involving thousands of genes was raised in T-cells. Finally, we showed that GPx inhibition reduced the DNA damaging effect of H2O2 in thyrocytes. We conjecture that defects of anti- H2O2 protection could promote spontaneous thyroid cancers. Here we characterize the response of thyrocytes to H2O2 from the perspective of DNA damage (SSB and DSB), cell death and genome-wide transcription. We adopted a dual comparative set up. First, in order to gain preliminary insights about which effects are specific to thyrocytes, all experiments were run in parallel in T-cells. Second, all experiments were replicated with radiation, providing a comparison with a proven etiological agent of PTCs. Hence, we investigated all 4 combinations of two factors: thyrocytes vs. T-cells and H2O2 vs. radiation. Cell lines divide indefinitively owning to basic dysfunctions of cell cycle controls. These have the potential to distort the stress response, DNA repair and cell death in particular. Hence, we worked exclusively on human primary cultures. The radiation and presumably also the H2O2 responses vary among individuals. We seek to average out individual effects by replicating the microarray experiments across the matched T-cells and thyrocytes of 8 donors.

			Action	DRS
	1h-Results.mzid.gz	Mzid
	1h_Ctrl-R1.mgf	Mgf
	1h_Ctrl-R1.raw	Raw
	1h_Ctrl-R2.mgf	Mgf
	1h_Ctrl-R2.raw	Raw

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Proteomic profiling of UV damage repair patches

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