Publications by authors named "G H Ira"

Formation of templated insertions at DNA double-strand breaks (DSBs) is very common in cancer cells. The mechanisms and enzymes regulating these events are largely unknown. Here, we investigated templated insertions in yeast at DSBs using amplicon sequencing across a repaired locus.

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In metazoans mitochondrial DNA (mtDNA) or retrotransposon cDNA released to cytoplasm are degraded by nucleases to prevent sterile inflammation. It remains unknown whether degradation of these DNA also prevents nuclear genome instability. We used an amplicon sequencing-based method in yeast enabling analysis of millions of DSB repair products.

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Article Synopsis
  • - The study investigates how templated insertions at DNA double-strand breaks (DSBs) occur in yeast, revealing that these insertions are usually short (5-34 base pairs) and formed through a foldback mechanism using microhomologies near the DSBs.
  • - The process relies on a hybrid mechanism where one end of the insertion requires DNA synthesis by Polδ, while the other end is linked through a nonhomologous end joining method, particularly affected in mutant strains with low RPA levels.
  • - The research suggests that the formation of these templated insertions, including complex ones with inverted sequences, may be heightened in cancer cells due to a shortage of RPA, which is associated with genomic instability.
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In metazoans release of mitochondrial DNA or retrotransposon cDNA to cytoplasm can cause sterile inflammation and disease . Cytoplasmic nucleases degrade these DNA species to limit inflammation . It remains unknown whether degradation these DNA also prevents nuclear genome instability.

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In metazoans release of mitochondrial DNA or retrotransposon cDNA to cytoplasm can cause sterile inflammation and disease. Cytoplasmic nucleases degrade these DNA species to limit inflammation. It remains unknown whether degradation these DNA also prevents nuclear genome instability.

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