Abstract
When we think about genetic influence of radiation, non-targeted effects of radiation is an important object. And we have to leave a conventional paradigm that a target of genetic effect of radiation is DNA. Influence of radiation does not appear as direct influence of radiation. Influence of radiation appears away from initial hit both in terms of time and space. This phenomenon is called genetic instability. However, induction mechanism is not made clear. This study planned to clarify how a p53 gene function contributed to genetic instability derivation. In this study, we used a primary culture cells derived from p53 gene normal (+/+) and knockout (-/-) C57B mouse. 106 cells were inoculated into T75 flask and each culture was subcultured at every 5day. As a result, the p53 normal cells grew with a growth rate 1 until passage 6 or 7 generations. However, the cells restored proliferation potency again when passage reached at 10. On the other hand, p53 knockout cells continued multiplying at growth rate 3.1-.53 lively without passing through temporary breeding degradation. Furthermore, we analyzed a change of chromosomal karyotype with increase of passage. The structural aberration was not seen in normal and knockout cells. However, we found that 35-40% of p53 knockout cells have 88 chromosomes. This means that p53 knockout cell is defective in chromosomal homeostasis maintenance mechanim. This shows that p53 plays an important role in chromosomal homeostasis maintenance.
