Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function

Article Abstract:

The molecular bases for the pigmentation phenotypes of variant extension locus alleles in mice was investigated. The results showed that the murine extension locus encodes the melanocyte-stimulating hormone (MSH) receptor. The recessive yellow allele is a frameshift mutation causing a prematurely terminated, nonfuntional receptor. The sombre and tobacco-darkening alleles, which have dominant melanizing effects, produce hyperactive receptors. These results suggest that point mutations alter MSH receptor function, thus producing pigmentation phenotypes of variant extension locus alleles.

Genetic aspects, Hormone receptors, Color of animals, Animal coloration, Intermedin, Melanocyte stimulating hormone

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Exocrine gland dysfunction in MC5-R-deficient mice: evidence for coordinated regulation of exocrine gland function by melanocortin peptides

Article Abstract:

The melanocortin peptide receptor MC5-R is found in many exocrine tissues. Genetic manipulation by targeted mutation using mice was done to investigate the function of melanocortin in exocrine gland regulation. Mutant mice had significant reduction of sebaceous lipid production resulting in defective water repulsion. There are numerous other functions attributed to melanocortin in the coordinated regulation of exocrine function. The regulatory mechanisms appear to be mediated by MC5-R.

Physiological aspects, Peptide hormones, Glands

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Targeted disruption of the melanocortin-4 receptor results in obesity in mice

Article Abstract:

The role of signaling through the melanocortin-4 receptor (MC4-R) in the regulation of body weight is investigated. Mice lacking the G-protein coupled receptor were produced by gene targeting in embryonic stem cells. Results reveal that the absence of the MC4-R leads to an obesity syndrome similar to the agouti syndrome. Results also support a model wherein the primary instrument by which agouti induces obesity is chronic antagonism of the MC4-R.

Obesity, G proteins

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