| Abstrakt: |
The viable yellow Avymutation results in a mottled yellow mouse that is obese, slightly larger than its nonyellow sibs, and more susceptible to tumor formation in those tissues sensitized by the strain genome. The mutation exhibits variable expressivity resulting in a continuum of coat color phenotypes, from clear yellow to pseudoagouti. The mouse agoutiprotein is a paracrine signaling molecule that induces hair follicle melanocytes to switch from the synthesis of black pigment to yellow pigment. Molecular cloning studies indicate that the obesity and growth effects of the Avymutation result from ectopic expression of the normal agoutigene product. This review seeks to summarize the current state of knowledge regarding the obesity, stimulation of somatic growth, and enhancement of tumor formation caused by the Avymutation, and to interpret these pleiotropic effects in terms of the normal function of the agoutiprotein.—Yen, T. T., Gill, A. M., Frigeri, L. G., Barsh, G. S., and Wolff, G. L. Obesity, diabetes, and neoplasia in yellow Avy/‐ mice: ectopic expression of the agoutigene. FASEB J.8: 479‐488; 1994. |
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