The delay in progression of X-irradiated cells through the cell cycle, which is more pronounced in normal (N) than in A-T fibroblasts, is greatest for cells in G2 at the time of irradiation. The greater effect of radiation on the initiation of DNA synthesis in N than in A-T cells is reflected in the shape of the percent labelled mitosis curves after 3H-thymidine treatment. The duration of the S phase in unirradiated A-T cells is greater than in N cells. Any explanation of the underlying defect in A-T must account not only for the reduced radiosensitivity of DNA synthesis but for the lesser delay in G2. Our data support the hypothesis that DNA is the principal target for radiation-induced G2 delay.
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http://dx.doi.org/10.1080/09553008214551661 | DOI Listing |
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