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Lymphocyte-specific compensation for XLF/cernunnos end-joining functions in V(D)J recombination
Gang Li1, Frederick W Alt, Hwei-Ling Cheng
1Howard Hughes Medical Institute, The Children's Hospital, The CBR Institute of Biomedical Research, Harvard Medical School, Boston, MA 02115, USA.
Molecular Cell
|September 9, 2008
Summary
XLF deficiency impairs DNA repair and V(D)J recombination in mouse cells. However, developing lymphocytes compensate for XLF loss, suggesting alternative repair pathways exist.
Area of Science:
- Molecular Biology
- Immunology
- Genetics
Background:
- Mutations in XLF/Cernunnos (XLF) are linked to human lymphocytopenia.
- XLF is proposed to function in classical nonhomologous end joining (C-NHEJ).
Purpose of the Study:
- To investigate the role of XLF in V(D)J recombination and DNA repair in mice.
- To understand XLF's contribution to lymphocyte development and immunoglobulin class switch recombination.
Main Methods:
- Analysis of XLF-deficient mouse embryonic fibroblasts and pro-B cell lines.
- Assessment of ionizing radiation (IR) sensitivity and V(D)J recombination efficiency.
- Evaluation of lymphocyte numbers and immunoglobulin heavy-chain class switch recombination in XLF-deficient mice.
Main Results:
- XLF-deficient fibroblasts show sensitivity to IR and impaired V(D)J recombination.
- Mature lymphocyte counts in XLF-deficient mice are only moderately reduced.
- Developing B cells exhibit near wild-type V(D)J recombination despite XLF deficiency.
- Mature B cells show defects in immunoglobulin heavy-chain class switch recombination.
Conclusions:
- XLF is implicated as a C-NHEJ factor.
- Developing mouse lymphocytes possess compensatory mechanisms for XLF loss during V(D)J recombination.
- Cell-type-specific factors or pathways contribute to lymphocyte development and DNA repair.
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