Pol32 is an accessory subunit of the replicative DNA Polymerase delta and of the translesion Polymerase zeta. Pol32 is involved in DNA replication, recombination and repair. Pol32's participation in high-and low-fidelity processes, together with the phenotypes arising from its disruption, imply multiple roles for this subunit within eukaryotic cells, not all of which have been fully elucidated. Using pol32 null mutants and two partial loss-of-function alleles pol32(rd1) and pol32(rds) in Drosophila melanogaster, we show that Pol32 plays an essential role in promoting genome stability. Pol32 is essential to ensure DNA replication in early embryogenesis and it participates in the repair of mitotic chromosome breakage. In addition we found that pol32 mutantssuppress position effect variegation, suggesting a role for Pol32 in chromatin architecture.

Loss of Pol32 in Drosophila melanogaster causes chromosome instability and suppresses variegation / Tritto, Patrizia; Palumbo, Valeria; Micale, Lucia; Marzulli, Marco; Bozzetti, Maria Pia; Specchia, Valeria; Palumbo, Gioacchino; Pimpinelli, Sergio; Berloco, Maria. - In: PLOS ONE. - ISSN 1932-6203. - 10:3(2015). [10.1371/journal.pone.0120859]

Loss of Pol32 in Drosophila melanogaster causes chromosome instability and suppresses variegation

Palumbo, Valeria;Pimpinelli, Sergio;
2015

Abstract

Pol32 is an accessory subunit of the replicative DNA Polymerase delta and of the translesion Polymerase zeta. Pol32 is involved in DNA replication, recombination and repair. Pol32's participation in high-and low-fidelity processes, together with the phenotypes arising from its disruption, imply multiple roles for this subunit within eukaryotic cells, not all of which have been fully elucidated. Using pol32 null mutants and two partial loss-of-function alleles pol32(rd1) and pol32(rds) in Drosophila melanogaster, we show that Pol32 plays an essential role in promoting genome stability. Pol32 is essential to ensure DNA replication in early embryogenesis and it participates in the repair of mitotic chromosome breakage. In addition we found that pol32 mutantssuppress position effect variegation, suggesting a role for Pol32 in chromatin architecture.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1658915
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