AI Article Synopsis
- The scid mutation in mice disrupts the normal development of immune cells, resulting in a lack of properly functioning B and T lymphocytes.
- Mice with the scid mutation are more susceptible to the harmful effects of ionizing radiation, showing increased rates of chromosome damage.
- The findings suggest that the challenges in chromosome repair mechanisms in scid mice may help researchers understand DNA repair processes in complex organisms.
Article Abstract
The murine severe combined immunodeficiency (scid) mutation interferes with normal recombination of immunoglobulin and T-cell receptor genes. This immunologic defect results in a lack of fully differentiated B and T cells in scid/scid mice. Animals homozygous for the scid mutation also display increased sensitivity to the damaging effects of ionizing radiation. We report here our observations of high frequencies of radiation-induced chromatid interchanges and intrachanges in bone marrow cells and fibroblasts from scid/scid mice. The presence of these aberrant chromosome structures suggests that a delay in strand rejoining underlies the increased sensitivity of scid/scid mice to ionizing radiation. The scid mutation may provide important clues for understanding the relationship between mitotic recombination and DNA repair in higher eukaryotic cells.
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| http://dx.doi.org/10.1159/000133196 | DOI Listing |
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