| Project/Area Number |
11640619
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
遺伝
|
|---|
| Research Institution | Saitama University |
|---|
Principal Investigator |
INOUE Hirokazu SAITAMA University, Fac. Science Dept. of Regulation-Biology, Professor, 理学部, 教授 (60114203)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ISHII Chizu SAITAMA University, Fac. Science Dept. of Regulation-Biology, Associate Professor, 理学部, 助教授 (00114215)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
|---|
| Keywords | recQ / DNA repair / Recombination / Neurospora / queling / mitochondria / Instability / aging / mus-10 / ミトコンドリアDNA / DNAシークエンス |
|---|
| Research Abstract |
Neurospora crassa has 2 recQ homolog genes, recQ1 and recQ2, which encode RecQ helicase. We disrupted those genes and characterized phenotypes. Gene recQ1 was same to mus-19 and also qde-3 genes. The mus-19 mutant is sensitive to MMS. EMS, MNNG, 4NQO and camptotecin. Epistasis analyzes showed that mus-19 belonged to recombination repair and postreplication repair. It did not show high mutation frequency and high recombination frequency. In the mus-19 strain we could not identify "quering" that is gene silencing in N. crassa. Also aging of the hyphae was not observed in this strain. Like the mus-19 strain, the recQ2 mutant was sensitive to mutagens. We are investigating other phenotype of this strain.
The mus-10 mutant grow normally after germination, but several days later the growth became slow and finally stopped. This strain was sensitive UV and MMS. Epistasis analyzes showed that combination with mus-18 become synergistic in mutagen sensitivity, but other combination did not. Telomere length did not change at the aging step. Some data showed this mutant had defect in mitochondria DNA stability.
|
