Loss of Pol32, a subunit of DNA polymerases δ and ζ, leads to different patterns of genome stability than direct impairment of these individual polymerases
mutants is substantially suppressed in strains that lack DNA polymerase ζ, suggesting that this error-prone polymerase may stimulate DNA breaks in conditions of DNA replication stress. Our studies are likely to have wide relevance since sequence variants of POLD3 (the human homolog of Pol32) are associated with certain types of human tumors.
Authors
- Xing-Xing Tang
- Ke Zhang (ORCID: https://orcid.org/0000-0001-9204-6556)
- Dao‐Qiong Zheng (ORCID: https://orcid.org/0000-0001-9365-2339)
- Yeke Wang (ORCID: https://orcid.org/0000-0003-1977-1254)
- Thomas D. Petes (ORCID: https://orcid.org/0000-0003-4890-8002)
- Lei Qi (ORCID: https://orcid.org/0009-0008-2488-453X)
- Min He
- Li-Yan Tian
- Ke-Jing Li
Institutions
- Dalian Ocean University (CN)
- Duke University (US)
- Zhejiang University (CN)
Publication Details
- Journal
- mBio
- Published
- 2026-04-17
- DOI
- https://doi.org/10.1128/mbio.00531-26
- Primary Topic
- DNA Repair Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China
- National Institutes of Health