PDIP38/PolDIP2 controls the DNA damage tolerance pathways by increasing the relative usage of translesion DNA synthesis over template switching.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2019
Historique:
received: 03 10 2018
accepted: 19 02 2019
entrez: 7 3 2019
pubmed: 7 3 2019
medline: 18 12 2019
Statut: epublish

Résumé

Replicative DNA polymerases are frequently stalled at damaged template strands. Stalled replication forks are restored by the DNA damage tolerance (DDT) pathways, error-prone translesion DNA synthesis (TLS) to cope with excessive DNA damage, and error-free template switching (TS) by homologous DNA recombination. PDIP38 (Pol-delta interacting protein of 38 kDa), also called Pol δ-interacting protein 2 (PolDIP2), physically associates with TLS DNA polymerases, polymerase η (Polη), Polλ, and PrimPol, and activates them in vitro. It remains unclear whether PDIP38 promotes TLS in vivo, since no method allows for measuring individual TLS events in mammalian cells. We disrupted the PDIP38 gene, generating PDIP38-/- cells from the chicken DT40 and human TK6 B cell lines. These PDIP38-/- cells did not show a significant sensitivity to either UV or H2O2, a phenotype not seen in any TLS-polymerase-deficient DT40 or TK6 mutants. DT40 provides a unique opportunity of examining individual TLS and TS events by the nucleotide sequence analysis of the immunoglobulin variable (Ig V) gene as the cells continuously diversify Ig V by TLS (non-templated Ig V hypermutation) and TS (Ig gene conversion) during in vitro culture. PDIP38-/- cells showed a shift in Ig V diversification from TLS to TS. We measured the relative usage of TLS and TS in TK6 cells at a chemically synthesized UV damage (CPD) integrated into genomic DNA. The loss of PDIP38 also caused an increase in the relative usage of TS. The number of UV-induced sister chromatid exchanges, TS events associated with crossover, was increased a few times in PDIP38-/- human and chicken cells. Collectively, the loss of PDIP38 consistently causes a shift in DDT from TLS to TS without enhancing cellular sensitivity to DNA damage. We propose that PDIP38 controls the relative usage of TLS and TS increasing usage of TLS without changing the overall capability of DDT.

Identifiants

pubmed: 30840704
doi: 10.1371/journal.pone.0213383
pii: PONE-D-18-28757
pmc: PMC6402704
doi:

Substances chimiques

Avian Proteins 0
Multifunctional Enzymes 0
Nuclear Proteins 0
POLDIP2 protein, human 0
DNA 9007-49-2
DNA Primase EC 2.7.7.-
DNA polymerase beta2 EC 2.7.7.-
PrimPol protein, human EC 2.7.7.-
DNA Polymerase beta EC 2.7.7.7
DNA-Directed DNA Polymerase EC 2.7.7.7
Rad30 protein EC 2.7.7.7

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0213383

Subventions

Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/H019723/1
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/M008800/1
Pays : United Kingdom

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Masataka Tsuda (M)

Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan.

Saki Ogawa (S)

Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Masato Ooka (M)

Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.

Kaori Kobayashi (K)

Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.

Kouji Hirota (K)

Department of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, Tokyo, Japan.

Mitsuo Wakasugi (M)

Faculty of Pharmacy, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.

Tsukasa Matsunaga (T)

Faculty of Pharmacy, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kanazawa, Japan.

Tetsushi Sakuma (T)

Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan.

Takashi Yamamoto (T)

Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan.

Shunsuke Chikuma (S)

Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.

Hiroyuki Sasanuma (H)

Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Michelle Debatisse (M)

Institut Curie UMR 3244, Universite Pierre et Marie Curie (Paris 06), CNRS Paris, France.

Aidan J Doherty (AJ)

Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, United Kingdom.

Robert P Fuchs (RP)

DNA Damage Tolerance CNRS, UMR7258, Marseille, France.
Institut Paoli-Calmettes, Marseille, France.
Aix-Marseille University, UM 105, Marseille, France.
Inserm, U1068, CRCM, Marseille, France.

Shunichi Takeda (S)

Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

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