- THIS ARTICLE
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- SERVICES
- Similar articles in this journal
- Similar articles in PubMed
- Alert me to new issues of the journal
- Download to citation manager
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Perry, W. L.
- Articles by Copeland, N. G.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Perry, W. L.
- Articles by Copeland, N. G.
Genetics, Vol 140, 267-274, Copyright © 1995
INVESTIGATIONS |
A Transgenic Mouse Assay for Agouti Protein Activity
W. L. Perry, C. M. Hustad, D. A. Swing, N. A. Jenkins and N. G. Copeland
Mammalian Genetics Laboratory, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702
The mouse agouti gene encodes an 131 amino acid paracrine signaling molecule that instructs hair follicle melanocytes to switch from making black to yellow pigment. Expression of agouti during the middle part of the hair growth cycle in wild-type mice produces a yellow band on an otherwise black hair. The ubiquitous unregulated expression of agouti in mice carrying dominant yellow alleles is associated with pleiotropic effects including increased yellow pigment in the coat, obesity, diabetes and increased tumor susceptibility. Agouti shows no significant homology to known genes, and the molecular analysis of agouti alleles has shed little new light on the important functional elements of the agouti protein. In this paper, we show that agouti expression driven by the human {beta}-ACTIN promoter produces obese yellow transgenic mice and that this can be used as an assay for agouti activity. We used this assay to evaluate a point mutation associated with the a(16H) allele within the region encoding agouti's putative signal sequence and our results suggest that this mutation is sufficient to cause the a(16H) phenotype. Thus, in vitro mutagenesis followed by the generation of transgenic mice should allow us to identify important functional elements of the agouti protein.
This article has been cited by other articles:
![]() |
K. Nakayama and T. Ishida Alu-mediated 100-kb deletion in the primate genome: The loss of the agouti signaling protein gene in the lesser apes. Genome Res., April 1, 2006; 16(4): 485 - 490. [Abstract] [Full Text] [PDF] |
||||
![]() |
Genetically Modified Animals in Endocrinology Endocr. Rev., June 1, 2004; 25(3): 512 - 519. [Full Text] [PDF] |
||||
![]() |
R. J. Miltenberger, K. Wakamatsu, S. Ito, R. P. Woychik, L. B. Russell, and E. J. Michaud Molecular and Phenotypic Analysis of 25 Recessive, Homozygous-Viable Alleles at the Mouse agouti Locus Genetics, February 1, 2002; 160(2): 659 - 674. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. L.K. Tamashiro, T. Wakayama, R. J. Blanchard, D. C. Blanchard, and R. Yanagimachi Postnatal Growth and Behavioral Development of Mice Cloned from Adult Cumulus Cells Biol Reprod, July 1, 2000; 63(1): 328 - 334. [Abstract] [Full Text] |
||||
![]() |
C. Quéva, G. A. McArthur, L. S. Ramos, and R. N. Eisenman Dwarfism and Dysregulated Proliferation in Mice Overexpressing the MYC Antagonist MAD1 Cell Growth Differ., December 1, 1999; 10(12): 785 - 796. [Abstract] [Full Text] |
||||
![]() |
R. J. Miltenberger, R. L. Mynatt, B. D. Bruce, W. O. Wilkison, R. P. Woychik, and E. J. Michaud An agouti mutation lacking the basic domain induces yellow pigmentation but not obesity in transgenic mice PNAS, July 20, 1999; 96(15): 8579 - 8584. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Miltenberger, R. L. Mynatt, J. E. Wilkinson, and R. P. Woychik The Role of the agouti Gene in the Yellow Obese Syndrome J. Nutr., September 1, 1997; 127(9): 1902 - 1902. [Abstract] [Full Text] |
||||
![]() |
R. A. Kesterson, D. Huszar, C. A. Lynch, R. B. Simerly, and R. D. Cone Induction of Neuropeptide Y Gene Expression in the Dorsal Medial Hypothalamic Nucleus in Two Models of the Agouti Obesity Syndrome Mol. Endocrinol., May 1, 1997; 11(5): 630 - 637. [Abstract] [Full Text] |
||||







