Mice that are homozygous for the targeted mutation are viable, fertile, but are 40-60% the size of normal mice. No <em>Xrcc5</em> protein product is detected. The growth deficiency phenotype is exhibited as early as E15.5. Organ weights, excepting lymphoid organs, are proportional to total body weight. Histological analysis shows decreased size of spleen, lymph nodes and thymus. T cell and B cell development is arrested at early precursor stages and a deficiency in V(D)J rearrangement is exhibited. B cell maturation stops at the B220+CD43+ stage. Only CD4-CD8- cells are found in the thymus. Primary embryonic fibroblasts (MEFs) have slower growth and early loss of proliferating cells. Early appearance of non-dividing cells in MEF cultures suggest early onset senescence. Karyotypes reveal increased chromosomal aberrations. Breaks or translocations occur in 83% of metaphases, polyploidy in 15%. Although cells from the mutant mice display chromosomal instability, these mice do not display early tumorigenesis. Litters must be fostered because homozygous mutant female mice are unable to sustain newborn pups. Survival of homozygous mutant mice is 80% when the larger heterozygous mutant and wildtype littermates are removed. This mutant mouse strain represents a model that may be useful in studies related to DNA repair and aging.

These <i> Xrcc5</i> knock-out mice exhibit growth deficiency including decreased size of spleen, lymph nodes and thymus with curtailed T cell and B cell development.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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