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

Pol32 is an accessory subunit of the replicative DNA Polymerase δ and of the translesion Polymerase ζ. 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 multi...

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Bibliographic Details
Published in:PloS one 2015-03, Vol.10 (3), p.e0120859-e0120859
Main Authors: Tritto, Patrizia, Palumbo, Valeria, Micale, Lucia, Marzulli, Marco, Bozzetti, Maria Pia, Specchia, Valeria, Palumbo, Gioacchino, Pimpinelli, Sergio, Berloco, Maria
Format: Article
Language:English
Subjects:
Alleles
Animals
Breakage
Chromatin
Chromosomal Instability
Chromosomes
Deoxyribonucleic acid
DNA
DNA biosynthesis
DNA damage
DNA polymerase
DNA repair
DNA-directed DNA polymerase
DNA-Directed DNA Polymerase - genetics
Drosophila
Drosophila melanogaster
Drosophila melanogaster - embryology
Drosophila melanogaster - genetics
Drosophila Proteins - genetics
Embryogenesis
Embryonic growth stage
Female
Genetics
Genomes
Insects
Metabolism
Mutants
Mutation
Position-effect variegation
Proteins
Recombination
Repair
Replication
Ribosomal DNA
Saccharomyces cerevisiae
Stability
Variegation
Yeast
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Summary:Pol32 is an accessory subunit of the replicative DNA Polymerase δ and of the translesion Polymerase ζ. 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 pol32rd1 and pol32rds 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 mutants suppress position effect variegation, suggesting a role for Pol32 in chromatin architecture.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0120859