Variable diversity joining recombination: nonhairpin coding ends in thymocytes of SCID and wild-type mice.

SCID and Wild-Type Mice Nonhairpin Coding Ends in Thymocytes of Variable Diversity Joining Recombination:

Transient restoration of gene rearrangement at multiple T cell receptor loci in gamma-irradiated scid mice

The developmental arrest of thymocytes from scid mice, deficient in variable, (diversity), and joining, or V(D)J recombination, can be overcome by sublethal gamma-irradiation. Since previous studies focused on restoration of rearrangement of the T cell receptor (TCR) beta locus, productive rearrangement of which is selected for, we sought to examine to what extent locus specificity and cellular...

Involvement of illegitimate V(D)J recombination or microhomology-mediated nonhomologous end-joining in the formation of intragenic deletions of the Notch1 gene in mouse thymic lymphomas.

Deregulated V(D)J recombination-mediated chromosomal rearrangements are implicated in the etiology of B- and T-cell lymphomagenesis. We describe three pathways for the formation of 5'-deletions of the Notch1 gene in thymic lymphomas of wild-type or V(D)J recombination-defective severe combined immune deficiency (scid) mice. A pair of recombination signal sequence-like sequences composed of hept...

Mouse Thymic Lymphomas Gene in Notch1 the Formation of Intragenic Deletions of the Microhomology-Mediated Nonhomologous End-Joining in Involvement of Illegitimate V(D)J Recombination or

Deregulated V(D)J recombination-mediated chromosomal rearrangements are implicated in the etiology of Band T-cell lymphomagenesis. We describe three pathways for the formation of 5 -deletions of the Notch1 gene in thymic lymphomas of wild-type or V(D)J recombination-defective severe combined immune deficiency (scid) mice. A pair of recombination signal sequence-like sequences composed of heptam...

Analyses of TCRB rearrangements substantiate a profound deficit in recombination signal sequence joining in SCID foals: implications for the role of DNA-dependent protein kinase in V(D)J recombination.

We reported previously that the genetic SCID disease observed in Arabian foals is explained by a defect in V(D)J recombination that profoundly affects both coding and signal end joining. As in C.B-17 SCID mice, the molecular defect in SCID foals is in the catalytic subunit of the DNA-dependent protein kinase (DNA-PKCS); however, in SCID mice, signal end resolution remains relatively intact. Mor...