| Project/Area Number |
13839004
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
ONO Tetsuya Tohoku University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (00107509)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
IKEHATA Hironobu Tohoku University, Graduate School of Medicine, Research Associate, 大学院・医学系研究科, 助手 (90250737)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | mouse / testis / germ-line cells / mutation / mismatch repair / deletion / 自然突然変異 / 減数分裂 / 精原細胞 / 精細胞 |
|---|
| Research Abstract |
In an attempt to elucidate if the spontaneous mutations occurring in germ cells are different from those in somatic tissues, we have analysed spontaneous mutant frequencies in testicular cells at infant and adult stages of lacZ-transgenic mice. The infant's testis is rich with spermatogonia, while adult's testis include all kinds of cells in spermatogesis. We have also analysed molecular nature of mutations by analyzing DNA sequence of mutants.
The mutant frequencies of testicular cells were similar to those in somatic tissues spch as brain and liver at both infant and adult stages. A comparison of the molecular nature of mutations between testicular cells and somatic cells, however, revealed that the frequency of deletion mutations which had direct repeat sequences at the break points and thus assumed to be originated from slippage of DNA polymerase, was lower in germ line cells than in somatic tissues. Since this kind of mutation are assumed to be suppressed, at least in part, by mismatch repair system, we analysed mutations in mismatch repair deficient mice. The frequencies of mutant appearance as well as slippage-type mutations were found to be elevated in the mice.
These results suggest an important role of mismatch repair system in suppressing the occurrence of spontaneous mutation in germ line cells.
|
