Heavy-ion beam (HIB) irradiation has been widely used in microbial mutation breeding. However, a global cellular response to such radiation remains mostly uncharacterised. In this study, we used transcriptomics to analyse the damage repair response in Saccharomyces cerevisiae following a semi-lethal HIB irradiation (80 Gy), which induced a significant number of DNA double-strand breaks. Our analysis of differentially expressed genes (DEGs) from 50 to 150 min post-irradiation revealed that upregulated genes were significantly enriched for gene ontology and Kyoto encyclopaedia of genes and genomes terms related to damage repair response. Based on the number of DEGs, their annotation, and their relative expression, we established that the peak of the damage repair response occurred 75 min post-irradiation. Moreover, we exploited the data from our recent study on X-ray irradiation-induced repair to compare the transcriptional patterns induced by semi-lethal HIB and X-ray irradiations. Although these two radiations have different properties, we found a significant overlap (> 50%) for the DEGs associated with five typical DNA repair pathways and, in both cases, identified homologous recombination repair (HRR) as the predominant repair pathway. Nevertheless, when we compared the relative enrichment of the five DNA repair pathways at the key time point of the repair process, we found that the relative enrichment of HRR was higher after HIB irradiation than after X-ray irradiation. Additionally, the peak stage of HRR following HIB irradiation was ahead of that following X-ray irradiation. Since mutations occur during the DNA repair process, uncovering detailed repair characteristics should further the understanding of the associated mutagenesis features.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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Evidence ID | Analyze ID | File | Description |
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