Targeting the FANCJ–BRCA1 interaction promotes a switch from recombination to polη-dependent bypass
Open accessAbstract
BRCA1 and the DNA helicase FANCJ (also known as BACH1 or BRIP1) have common functions in breast cancer suppression and DNA repair. However, the functional significance of the direct interaction between BRCA1 and FANCJ remains unclear. Here, we have discovered that BRCA1 binding to FANCJ regulates DNA damage repair choice. Thus, when FANCJ binding to BRCA1 is ablated, the molecular mechanism chosen for the repair of damaged DNA is dramatically altered. Specifically, a FANCJ protein that cannot be phosphorylated at serine 990 or bind BRCA1 inhibits DNA repair via homologous recombination and promotes poleta-dependent bypass. Furthermore, the poleta-dependent bypass promoted by FANCJ requires the direct binding to the mismatch repair (MMR) protein, MLH1. Together, our findings implicate that in human cells BRCA1 binding to FANCJ is critical to regulate DNA repair choice and promote genomic stability. Moreover, unregulated FANCJ function could be associated with cancer and/or chemoresistance.
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Overexpression of K52R reduced homologous recombination after double-strand break induction.
“In particular, overexpression of the helicase-inactive K52R mutant in cells with wild-type FANCJ resulted in the accumulation of unrepaired DNA breaks when analyzed by pulse field electrophoresis [8], as well as reduced homologous recombination following double strand break induction [69].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
BRCA1 binding to FANCJ is essential for regulating the mechanism of DNA damage repair.
“More recently, it was shown that BRCA1 binding to FANCJ was essential for regulating the mechanism of DNA damage repair.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
FANCJ-deficient cells are sensitive to cisplatin, as are BRCA-deficient cells.
“similar to BRCA-deficient cells, FANCJ-deficient cells are sensitive to cisplatin [69]”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
The FANCJ S990A mutant reduces error-free homologous recombination repair and enhances error-prone DNA damage bypass through the Pol-η translesion synthesis polymerase.
“In particular, the FANCJ S990A mutant reduced error-free repair by homologous recombination and enhanced error-prone DNA damage bypass through the Pol-η translesion synthesis polymerase [69].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
Cells expressing the BRCA1 interaction-defective FANCJ mutant S990A show reduced DNA repair, similar to cells with the enzyme-inactivating FANCJ mutant K52R.
“Cells expressing the BRCA1 interaction- defective mutant S990A had reduced DNA repair, similar to an enzyme-inactivating FANCJ mutant, K52R.”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
Loss of FANCJ binding to BRCA1 enhances DNA damage tolerance.
“loss of FANCJ binding to BRCA1 also enhanced DNA damage tolerance [69]”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [69]
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Self-citation
- Authors
- Xie, J., Litman, R., Wang, S., Peng, M., Guillemette, S., Rooney, T., & Cantor, S. B.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Cantor, S B
- Venue
- Oncogene
- Published
- 2010-02-22
- Volume
- 29
- Issue
- 17
- Pages
- 2499-2508
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- PMC
- PMC2909592
- OpenAlex
- W2092435713
- Cited by
- 60
- References
- 43
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 1 · 2021: 4 · 2020: 4 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 6 · 2015: 2 · 2014: 6 · 2013: 4 · 2012: 8
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA129514)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- FANCJ, BRCA1, BACH1, BRIP1, homologous recombination, Pol eta, translesion synthesis, MLH1, DNA mismatch repair, genome stability, breast cancer, chemoresistance
- MeSH terms
- MutL Protein Homolog 1, Y-Family DNA Polymerases, DNA Damage, DNA-Directed DNA Polymerase, DNA Repair, Humans, Nuclear Proteins, Recombination, Genetic, Mitomycin, Drug Resistance, Neoplasm, BRCA1 Protein, Genomic Instability, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, Basic-Leucine Zipper Transcription Factors, Fanconi Anemia Complementation Group Proteins
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