Genetic studies of the mouse mutations mahogany and mahoganoid.
Genetic studies of the mouse mutations mahogany and mahoganoid.
复制标题
小鼠突变桃花心木和桃花心木的基因研究。
DOI：
10.1093/genetics/146.4.1407
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发表时间：
1997
期刊：
影响因子：
3.3
通讯作者：
Barsh,GS
中科院分区：
文献类型：
--
作者：
Miller,KA;Gunn,TM;Carrasquillo,MM;Lamoreux,ML;Galbraith,DB;Barsh,GS
The mouse mutationsmahogany (mg)andmahoganoid (md)are negative modifiers of theAgouticoat color gene, which encodes a paracrine signaling molecule that induces a switch in melanin synthesis from eumelanin to pheomelanin. Animals mutant formdormgsynthesize very little or no pheomelanin depending onAgoutigene background. The Agouti protein is normally expressed in the skin and acts as an antagonist of the melanocyte receptor for α-MSH (Mc1r); however, ectopic expression ofAgouticauses obesity, possibly by antagonizing melanocortin receptors expressed in the brain. To investigate wheremdandmglie in a genetic pathway with regard to Agouti and Mc1r signaling, we determined the effects of these mutations in animals that carried either a loss-of-function Mc1r mutation (recessive yellow, Mc1re) or a gain-of-functionAgoutimutation (lethal yellow, Ay). We found that theMc1remutation suppressed the effects ofmdandmg,but thatmdandmgsuppressed the effects ofAyon both coat color and obesity. Plasma levels of α-MSH and of ACTH were unaffected bymdormg.These results suggest thatmdandmginterfere directly with Agouti signaling, possibly at the level of protein production or receptor regulation.
