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

Tritto, P and Palumbo, V and Micale, L and Marzulli, M and Bozzetti, MP and Specchia, V and Palumbo, G and Pimpinelli, S and Berloco, M (2015) Loss of Pol32 in Drosophila melanogaster causes chromosome instability and suppresses variegation. PLoS ONE, 10 (3).

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Abstract

© 2015 Tritto et al. 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 mutantssuppress position effect variegation, suggesting a role for Pol32 in chromatin architecture.


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Tritto, P
Palumbo, V
Micale, L
Marzulli, Mmam341@pitt.eduMAM341
Bozzetti, MP
Specchia, V
Palumbo, G
Pimpinelli, S
Berloco, M
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorCotterill, SueUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 31 March 2015
Date Type: Publication
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Journal or Publication Title: PLoS ONE
Volume: 10
Number: 3
DOI or Unique Handle: 10.1371/journal.pone.0120859
Institution: University of Pittsburgh
Schools and Programs: School of Medicine > Microbiology and Molecular Genetics
Refereed: Yes
Date Deposited: 23 Aug 2016 14:01
Last Modified: 02 Feb 2019 14:55
URI: http://d-scholarship.pitt.edu/id/eprint/28489

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