Mice reconstituted with DNA polymerase beta-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normally - PubMed (original) (raw)
Mice reconstituted with DNA polymerase beta-deficient fetal liver cells are able to mount a T cell-dependent immune response and mutate their Ig genes normally
G Esposito et al. Proc Natl Acad Sci U S A. 2000.
Abstract
The ubiquitously expressed, error-prone DNA polymerase beta (polbeta) plays a role in base excision repair, and the involvement of this molecule in the nonhomologous end joining (NHEJ) process of DNA repair has recently been demonstrated in yeast. Polbeta-deficient mice are not viable, and studies on conditional mutants revealed a competitive disadvantage of polbeta(-/-) vs. wild-type cells. We show here that polbeta-deficient mice survive up to day 18.5 postcoitum, but die perinatally; a circumstance that allowed the investigation of a potential role of polbeta in lymphocyte development by transfer of fetal liver cells (FLC) derived from polbeta(-/-) embryos into lethally irradiated hosts. FLC transfers using mutant cells lead to an almost normal reconstitution of the lymphocyte compartment, indicating that polbeta-deficiency does not prevent V(D)J recombination, which is known to employ factors of the NHEJ pathway. Mice reconstituted with polbeta(-/-) FLC mount a normal T cell-dependent immune response against the hapten (4-hydroxy-3-nitrophenyl) acetyl (NP). Moreover, germinal center B cells from NP-immunized reconstituted mice show normal levels and patterns of somatic point mutations in their rearranged antibody genes, demonstrating that polbeta is not critically involved in somatic hypermutation.
Figures
Figure 1
polβ−/− embryos (Right) at day 18.5 p.c. are growth retarded compared with their polβ+/− (Center) and polβ+/+ (Left) littermates. Homozygous mutant embryos appeared to be cyanotic.
Figure 2
Lethally irradiated recipient 129/Sv mice were reconstituted with 106 FLC prepared from day 18.5 p.c. polβ+/− (●) and polβ−/− (○) embryos. One and two months after reconstitution, the total number of thymocytes, splenocytes, and femur bone marrow cells (A) was determined as well as the number of splenic B220+ B cells, CD4+ T cells, and CD8+ T cells (B).
Figure 3
Pattern of nucleotide exchanges in the V186.2 rearrangements of GC B cells derived from a wild-type C57BL/6 mouse and from mice reconstituted with wild-type and polβ-deficient day 18.5 p.c. FLC, respectively. n, the number of mutations; shared mutations in clonally related sequences were counted only once. The G to T exchange in codon 33, which represents a result of selection for NP-binding, was not considered to avoid skewing of the analysis (see text). Ts., transitions; Tv., transversions; Ts./Tv., the transitions over transversions ratio.
Similar articles
- Relative contribution of T and B cells to hypermutation and selection of the antibody repertoire in germinal centers of aged mice.
Yang X, Stedra J, Cerny J. Yang X, et al. J Exp Med. 1996 Mar 1;183(3):959-70. doi: 10.1084/jem.183.3.959. J Exp Med. 1996. PMID: 8642299 Free PMC article. - V(D)J recombinase activity in a subset of germinal center B lymphocytes.
Han S, Dillon SR, Zheng B, Shimoda M, Schlissel MS, Kelsoe G. Han S, et al. Science. 1997 Oct 10;278(5336):301-5. doi: 10.1126/science.278.5336.301. Science. 1997. PMID: 9323211 - DNA polymerase beta is able to repair breaks in switch regions and plays an inhibitory role during immunoglobulin class switch recombination.
Wu X, Stavnezer J. Wu X, et al. J Exp Med. 2007 Jul 9;204(7):1677-89. doi: 10.1084/jem.20070756. Epub 2007 Jun 25. J Exp Med. 2007. PMID: 17591858 Free PMC article. - Fidelity and infidelity in commitment to B-lymphocyte lineage development.
Rolink AG, Schaniel C, Busslinger M, Nutt SL, Melchers F. Rolink AG, et al. Immunol Rev. 2000 Jun;175:104-11. Immunol Rev. 2000. PMID: 10933595 Review. - Mouse models to explore the biological and organismic role of DNA polymerase beta.
Sobol RW. Sobol RW. Environ Mol Mutagen. 2024 Apr;65 Suppl 1(Suppl 1):57-71. doi: 10.1002/em.22593. Environ Mol Mutagen. 2024. PMID: 38619421 Free PMC article. Review.
Cited by
- The role of DNA polymerase activity in human non-homologous end joining.
Pospiech H, Rytkönen AK, Syväoja JE. Pospiech H, et al. Nucleic Acids Res. 2001 Aug 1;29(15):3277-88. doi: 10.1093/nar/29.15.3277. Nucleic Acids Res. 2001. PMID: 11470886 Free PMC article. - Transcription, beta-like DNA polymerases and hypermutation.
Reynaud CA, Frey S, Aoufouchi S, Faili A, Bertocci B, Dahan A, Flatter E, Delbos F, Storck S, Zober C, Weill JC. Reynaud CA, et al. Philos Trans R Soc Lond B Biol Sci. 2001 Jan 29;356(1405):91-7. doi: 10.1098/rstb.2000.0753. Philos Trans R Soc Lond B Biol Sci. 2001. PMID: 11205336 Free PMC article. Review. - Somatic immunoglobulin hypermutation.
Diaz M, Casali P. Diaz M, et al. Curr Opin Immunol. 2002 Apr;14(2):235-40. doi: 10.1016/s0952-7915(02)00327-8. Curr Opin Immunol. 2002. PMID: 11869898 Free PMC article. Review. - Immunoglobulin somatic hypermutation: double-strand DNA breaks, AID and error-prone DNA repair.
Wu X, Feng J, Komori A, Kim EC, Zan H, Casali P. Wu X, et al. J Clin Immunol. 2003 Jul;23(4):235-46. doi: 10.1023/a:1024571714867. J Clin Immunol. 2003. PMID: 12959216 Free PMC article. Review. - New insights into abasic site repair and tolerance.
Thompson PS, Cortez D. Thompson PS, et al. DNA Repair (Amst). 2020 Jun;90:102866. doi: 10.1016/j.dnarep.2020.102866. Epub 2020 Apr 30. DNA Repair (Amst). 2020. PMID: 32417669 Free PMC article. Review.
References
- Sobol R W, Horton J K, Kühn R, Gu H, Singhal R K, Prasad R, Rajewsky K, Wilson S H. Nature (London) 1996;379:183–186. - PubMed
- Wilson T E, Lieber M R. Proc Natl Acad Sci USA. 1999;33:23599–23609.
- Kunkel T A, Alexander P S. J Biol Chem. 1986;261:160–166. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical
Molecular Biology Databases
Miscellaneous