Project/Area Number |
18570209
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Developmental biology
|
Research Institution | Tokuyama College of Technology |
Principal Investigator |
AMANAI Kazuhito Tokuyama College of Technology, Liberal Arts Division, Professor (20390502)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,980,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | morphogenesis / signal transduction / ubiquitin protein ligase / Drosophila / ショウジョウバエ / ヘッジホッグ |
Research Abstract |
The product of the hyperplastic discs (byd) gene of Drosophila, HIT, is required for regulating imaginal disc cell proliferation and pattern formation. Sequence comparisons revealed that HYD contains a region similar to the putative catalytic domain of E6-AP, a cellular protein that associates with a human papillomavirus protein of E6-P, E6-E6-P has ubiquitin-protein ligase activity. As evidence that HYD is functionally similar to E6-P, we show that HYD associates with a Drosophila ubiquitin conjugating enzyme encoded by the bendless gene and that HYD forms a thioester with ubiquitin in a reaction dependent on this E2 enzyme. Mutation in the gene encoding an ubiquitin activating enzyme, in bendless, and in a gene encoding a proteasome component fins26, enhance the phenotype of hyd mutations suggesting that the products of these genes work together to control ubiquitinatin and subsequent degradation of proteins required for cell proliferation and pattern formation in Drosophila imaginal discs.
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