A critical role for DNA end-joining proteins in both lymphogenesis and neurogenesis
Open accessAbstract
XRCC4 was identified via a complementation cloning method that employed an ionizing radiation (IR)-sensitive hamster cell line. By gene-targeted mutation, we show that XRCC4 deficiency in primary murine cells causes growth defects, premature senescence, IR sensitivity, and inability to support V(D)J recombination. In mice, XRCC4 deficiency causes late embryonic lethality accompanied by defective lymphogenesis and defective neurogenesis manifested by extensive apoptotic death of newly generated postmitotic neuronal cells. We find similar neuronal developmental defects in embryos that lack DNA ligase IV, an XRCC4-associated protein. Our findings demonstrate that differentiating lymphocytes and neurons strictly require the XRCC4 and DNA ligase IV end-joining proteins and point to the general stage of neuronal development in which these proteins are necessary.
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Mutations in DNA repair pathway components lead to neurodevelopment and neurodegenerative diseases.
“mutations in DNA repair pathway components lead to neurodevelopment and neurodegenerative diseases”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [108]
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- Authors
- Gao, Y., Sun, Y., Frank, K. M., Dikkes, P., Fujiwara, Y., Seidl, K. J., Sekiguchi, J. M., Rathbun, G. A., Swat, W., Wang, J., Bronson, R. T., Malynn, B. A., Bryans, M., Zhu, C., Chaudhuri, J., Davidson, L., Ferrini, R., Stamato, T., Orkin, S. H., Greenberg, M. E., & Alt, F. W.
- Affiliations
- Howard Hughes Medical Institute (US)
- Boston Children's Hospital (US)
- Kyushu University (JP)
- Tufts University (US)
- Lankenau Medical Center (US)
- Corresponding author
- Alt, Frederick W.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1998-12
- Volume
- 95
- Issue
- 7
- Pages
- 891-902
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2109456034
- Cited by
- 688
- References
- 47
- Citations by year
- 2026: 10 · 2025: 14 · 2024: 11 · 2023: 7 · 2022: 9 · 2021: 13 · 2020: 36 · 2019: 16 · 2018: 15 · 2017: 22 · 2016: 28 · 2015: 18 · 2014: 22 · 2013: 20 · 2012: 28
- FWCI
- 14.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- National Institutes of Health (7k08ai001428-05)
- National Institute of Allergy and Infectious Diseases (AI 35714, AI01428, AI 20047, P01AI035714)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- XRCC4, DNA ligase IV, DNA end joining, neurogenesis, V(D)J recombination, radiosensitivity, premature senescence, embryonic lethality, neuronal apoptosis, postmitotic neurons, lymphocyte differentiation
- MeSH terms
- Ku Autoantigen, DNA Ligase ATP, Animals, Cell Cycle, Cell Differentiation, Cell Line, Central Nervous System, DNA Repair, DNA Helicases, DNA-Binding Proteins, Embryonic and Fetal Development, Fibroblasts, Neurons, Nuclear Proteins, DNA Ligases, Radiation, Ionizing, Gene Rearrangement, Lymphocyte Subsets, Apoptosis, Mice, Knockout, Body Patterning, Genes, Essential, Antigens, Nuclear, Mice
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