ATM stabilizes DNA double-strand-break complexes during V(D)J recombination

Article Abstract:

The study of Ataxia-telangiectasia mutated (ATM) shows that they function directly in the repair of chromosomal DNA double strand break by maintaining DNA ends in repair complexes generated during lymphocyte antigen receptor gene assembly. The findings when coupled with cell-cycle checkpoint and pro-apoptotic activities of ATM provide a molecular explanation for the increase in lymphoid tumors with translocations involving antigen receptor loci associated with ataxia-telangiectasia.

Science & research, Pennsylvania, Health aspects, Analysis, Causes of, DNA repair, Lymphoid tissue, Ataxia telangiectasia, Exon (Molecular genetics), Exons (Molecular genetics)

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Late embryonic lethality and impaired V(D)J recombination in mice lacking DNA ligase IV

Article Abstract:

DNA-end-joining reactions used in repair have common factors, including components of DNA-dependent protein kinase (DNA-PK), and Ku70-Ku80- and XRCC4. XRCC5 is known to interact with DNA ligase IV. The inactivation of the ligase IV gene in mice is shown to result in late embryonic lethality. V(D)J joining does not occur and ligase IV-deficient embryonic fibroblasts are sensitive to ionizing radiation, premature senescence and growth defects.

Protein kinases, Ligases

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Recombination signal sequences restrict chromosomal V(D)J recombination beyond the 12/23 rule

Article Abstract:

It has been possible to use embryonic stem cells and mice with a modified T-cell receptor (TCR)beta locus containing only one D-beta gene segment and one J-beta gene cluster to indicate that the 5' D-beta-1 12-recombination signal sequence, but not the J-beta-1 12-recombination signal sequences, targets rearrangement of a diverse V-beta repertoire.

T cell antigen receptors, Genetic recombination, T cells

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