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Transcription-coupled repair in Drosophila melanogaster is independent of the mismatch repair pathway

View ORCID ProfileLauri Törmä, View ORCID ProfileClaire Burny, View ORCID ProfileViola Nolte, View ORCID ProfileKirsten-André Senti, View ORCID ProfileChristian Schlötterer
doi: https://doi.org/10.1101/2020.04.07.029033
Lauri Törmä
1Institut für Populationsgenetik, Vetmeduni Vienna, Vienna, Austria
2Vienna Graduate School of Population Genetics, Vetmeduni Vienna, Vienna, Austria
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  • ORCID record for Lauri Törmä
Claire Burny
1Institut für Populationsgenetik, Vetmeduni Vienna, Vienna, Austria
2Vienna Graduate School of Population Genetics, Vetmeduni Vienna, Vienna, Austria
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Viola Nolte
1Institut für Populationsgenetik, Vetmeduni Vienna, Vienna, Austria
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Kirsten-André Senti
1Institut für Populationsgenetik, Vetmeduni Vienna, Vienna, Austria
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Christian Schlötterer
1Institut für Populationsgenetik, Vetmeduni Vienna, Vienna, Austria
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  • ORCID record for Christian Schlötterer
  • For correspondence: christian.schloetterer@vetmeduni.ac.at
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Abstract

Transcription-coupled repair (TCR) removes base damage on the transcribed strand of a gene to ensure a quick resumption of transcription. Based on the absence of key enzymes for TCR and empirical evidence, TCR was thought to be missing in Drosophila melanogaster. The recent demonstration of TCR in S2 cells raises the question about the involved genes. Since the mismatch repair (MMR) pathway serves a central role in TCR, at least in Escherichia coli, we studied the mutational signatures in flies with a deletion of the MMR gene spellchecker1 (spel1), a MutS homolog. Whole-genome sequencing of mutation accumulation (MA) lines obtained 7,345 new single nucleotide variants (SNVs) and 5,672 short indel mutations, the largest data set from an MA study in D. melanogaster. Based on the observed mutational strand-asymmetries, we conclude that TCR is still active without spel1. The operation of TCR is further confirmed by a negative association between mutation rate and gene expression. Surprisingly, the TCR signatures are detected for introns, but not for exons. We propose that an additional exon-specific repair pathway is masking the signature of TCR. This study presents the first step towards understanding the molecular basis of TCR in Drosophila melanogaster.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted April 08, 2020.
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Transcription-coupled repair in Drosophila melanogaster is independent of the mismatch repair pathway
Lauri Törmä, Claire Burny, Viola Nolte, Kirsten-André Senti, Christian Schlötterer
bioRxiv 2020.04.07.029033; doi: https://doi.org/10.1101/2020.04.07.029033
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Transcription-coupled repair in Drosophila melanogaster is independent of the mismatch repair pathway
Lauri Törmä, Claire Burny, Viola Nolte, Kirsten-André Senti, Christian Schlötterer
bioRxiv 2020.04.07.029033; doi: https://doi.org/10.1101/2020.04.07.029033

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