| Project/Area Number |
11672252
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Human genetics
|
|---|
| Research Institution | Nagasaki University School of Medicine |
|---|
Principal Investigator |
YOSHIURA Koh-ichiro Department of Human Genetics, Nagasaki University School of Medicine Associate Professor, 医学部, 助手 (00304931)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NIIKAWA Norio Nagasaki University School of Medicine Professor, 医学部, 教授 (00111170)
|
|---|
| Project Period (FY) |
1999 – 2000
|
| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
|---|
| Keywords | Hmx-1 / Homozygote / Lethal / Rescue / Genetic Background / Neural Crest cell / Hmx1 / Rescure / in situ Hybridization 法 / 致死性遺伝子 |
|---|
| Research Abstract |
The three genes of the murine Hmx family, designated Hmx1, Hmx2, and Hmx3, are expressed in the sensory nerve and uterus that suggest a functional role in development of those organs and/or pregnancy. The Hmx3 knockout mice, as suspected by the expressed region, show abnormal structure of inner ear and implantation defect in homozygote mice. To analyze the function of Hmx1 gene in the organ development and pregnancy, we adopted the homologous recombination technique. Homozygous targeted disruption of Hmx1 gene result in lethality at embryonic day 6-7 in intercross of F1 (129/Sv : C57BL/6) heterozygote. But this lethality is rescued in F2 or F3 intercross. This phenomenon suggest that rescue gene may exist in C57BL/6 mice genome. In the present state, however, it is unclear whether the genotype of mother or embryo could rescue the lethal phenotye. Once homozygote mice develop beyond the E5-E7 critical date, they are completely normal even in the tissues in which Hmx1 is expressed.
|
