ArticlePLoS genetics2019
The processivity factor Pol32 mediates nuclear localization of DNA polymerase delta and prevents chromosomal fragile site formation in Drosophila development.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- DNA polymerase delta governs parental histone transfer to DNA replication lagging strand.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Impacts of Sex Ratio Meiotic Drive on Genome Structure and Function in a Stalk-Eyed Fly.Genome biology and evolution · 2023Article
- Article
- Association of Mutations in Replicative DNA Polymerase Genes with Human Disease: Possible Application ofInternational journal of molecular sciences · 2023Review
- Under the magnifying glass: The ups and downs of rDNA copy number.Seminars in cell & developmental biology · 2023Review
- The DEAD-Box Protein Rok1 Coordinates Ribosomal RNA Processing in Association with Rrp5 inInternational journal of molecular sciences · 2022Article
- NovelJournal of medical genetics · 2022Article
- The stabilized Pol31-Pol3 interface counteracts Pol32 ablation with differential effects on repair.Life science alliance · 2021Article
- Genomic instability and cancer: lessons fromOpen biology · 2020Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The Pol32 protein is one of the universal subunits of DNA polymerase δ (Pol δ), which is responsible for genome replication in eukaryotic cells. Although the role of Pol32 in DNA repair has been well-characterized, its exact function in genome replication remains obscure as studies in single cell systems have not established an essential role for Pol32 in the process. Here we characterize Pol32 in the context of Drosophila melanogaster development. In the rapidly dividing embryonic cells, loss of Pol32 halts genome replication as it specifically disrupts Pol δ localization to the nucleus. This function of Pol32 in facilitating the nuclear import of Pol δ would be similar to that of accessory subunits of DNA polymerases from mammalian Herpes viruses. In post-embryonic cells, loss of Pol32 reveals mitotic fragile sites in the Drosophila genome, a defect more consistent with Pol32's role as a polymerase processivity factor. Interestingly, these fragile sites do not favor repetitive sequences in heterochromatin, with the rDNA locus being a striking exception. Our study uncovers a possibly universal function for DNA polymerase ancillary factors and establishes a powerful system for the study of chromosomal fragile sites in a non-mammalian organism.
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