Physiological consequences of ectopic agouti gene expression: the yellow obese mouse syndrome.
This review summarizes primary and downstream phenotypic manifestations, with emphasis on altered responsiveness to environmental stimuli, of dominant yellow mutations at the mouse agouti locus. Obvious effects include hyperinsulinemia, obesity, stimulation of somatic growth and tumorigenesis, and coat color. Downstream influences of hyperinsulinemia and obesity on the individual's physiology determine important components of the obese yellow agouti mouse syndrome. Collectively, the phenotypic aberrations described support the concept that identical genomes are expressed in a spectrum of physiological phenotypes that reflect the complex interdependence of gene-regulated physiological pathways and processes in the organism throughout extended, but temporally ordered, periods of fetal and neonatal development and aging. This summary identifies important areas for additional research and provides integrated information required for a systematic approach to the development of interventions for common adult human health problems.
Wolff
G L
GL
Division of Biochemical Toxicology, National Center for Toxicological Research/Food and Drug Administration, Jefferson 72079, USA. gwolff@nctr.fda.gov
Roberts
D W
DW
Mountjoy
K G
KG
D054366:Agouti Signaling Protein; D000818:Animals; D005786:Gene Expression Regulation; D006200:Hair Color / Q000235:genetics*; D036341:Intercellular Signaling Peptides and Proteins; D051379:Mice; D009765:Obesity / Q000235:genetics* / Q000473:pathology; D011506:Proteins / Q000235:genetics*; D013577:Syndrome
D054366:Agouti Signaling Protein; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins