2007 Fiscal Year Final Research Report Summary
Molecular mechanism for intercellular interactions involved in cardiovascular a〓craniofacial development
| Project/Area Number |
18590802
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KURIHARA Yukiko The University of Tokyo, Graduate School of Medicine, Assistant Professor (80345040)
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| Co-Investigator(Kenkyū-buntansha) |
KURIHARA Hiroki The University of Tokyo, Graduate School of Medicine, Professor (20221947)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Endothelin / Knock-In mouse / Cardiovascular development / Morphogenesis |
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| Research Abstract |
Cardiovascular and craniofacial development in vertebrates is a complex process involving the coordinated interaction of different cell populations. To elucidate how cell-cell interactions operate cell differentiation and organogenesis, cardiovascular and craniofacial development serves as a good model. Our previous study has revealed that Endothelin-1/Endothelin A receptor (ETAR) signal was essential for cranial and cardiac neural crest cell-derived tissue development(Nature 368, 703, 1994). In this study, we have established ETAR knock-in mice in which genes of interested can be expressed under the ETAR promoter by recombinase mediated cassette exchange (RMCE), and have used this system for analysis as follows.
1. Knock-in of ETAR cDNA The ETAR-null phenotype was completely rescued in ETAR-/cETAR mice. Cardiovascular and craniofacial abnormalities were normalized, suggesting that this RMCE system functioned well in the ETAR gene.
2. Knock-in of marker genes The lacZ expression in ETAR+/lacZ mice almost recapitulates the expression of ETAR mRNA revealed by whole-mount in situ hybridization. Moreover, ETAR expressing cells except for neural crest cells were i
3. Knock-in of ETAR-/ETBR ETAR has been considered to be largely equivalent to ETBR in terms of Gq/11-mediated signaling in in
4. Knock-in of other genes We are establishing mice in terms of Gq/11-mediated signaling in which ETARs are ubiquitously activate
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