| Summary: | 碩士 === 國立清華大學 === 輻射生物研究所 === 83 === Understanding of the molecular mechanism of radiation sen
sitivity in mammalian cells is important both in clinical and
basic research.The wild type Chinese hamster ovary(CHO)K1 cell
line and its x-ray sensitive mutant xrs-6 were used as the
model for this purpose.In addition to x-ray, this mutant is
cross-sensitive to other DNA-damaging agents, such as UV,MMS
and EMS.It has been shown that xrs-6 mutant was defective in
rejoining DNA double strand break(dsb)and in expression of 11
genes.Recently,the defect in repairing DNA dsb was found due to
lack of the DNA-end binding(DEB) activity resulted from the
deficiency of Ku80 protein.In this work, a spontaneous
revertant SR-16 from xrs-6 was isolated in order to futher
characterize the mutation. The SR-16 revertant was found to
have the same sensitivity to x-ray and UV as CHO-K1 cells, but
was still sensitive to MMS and EMS. Furthermore, SR-16 cells
had the same DEB activity and DNA dsb repair capacity as the
CHO-K1 cells. The results suggest that the mechanism of radio-
resistance in SR-16 is the same as in CHO-K1 cells and further
confirm the deficiency of Ku is responsible for the x-
raynsitive phenotype of the xrs-6 mutant. The level of 11 mRNAs
in SR-16 cells did not go back to the same level as in the CHO-
K1 cell line. The expression of those 11 mRNAs is there- fore
not regulated by Ku, although Ku protein has been shown to be
able to regulate transcription. The results also suggest that
there may be a common point between the repair of damages
caused by x-ray and UV, and Ku is involved in both repair
pathway.
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