Recent Biochemical Insights into Puberty Acceleration, Estrus Induction, and Puberty Delay in the House Mouse

Abstract

The mouse primer pheromones have received considerable attention since the 1960s. We have demonstrated that two unique androgen-dependent urinary metabolites, 3,4-dehydro-exo-bre-vicomin and 2-sec-butyldihydrothiazole, are effective in promoting estrus synchronization with a stereospecific response. Yet another unique metabolite, 6-hydroxy-6-methyl-3-heptanone has a strong puberty-accelerating activity. We now demonstrate that several androgen-dependent compounds are capable of accelerating the onset of puberty independently: 6-hydroxy-6-methyl-3-heptanone;2-sec-butyldihydrothiazole;3,4-dehydro-exo-brevicomin; α- and β-farnesenes. All have one characteristic in common: binding affinity to the major urinary protein (MUP). Based on our recent data, at least some controversies in the literature can be explained. The farnesenes originating from the preputial gland are also effective in estrus induction. A recombinant MUP devoid of its natural ligands has no biological activity. The function of MUP as a slow-release pheromone mediator appears plausible. There are structural similarities between MUP and the pheromone-binding proteins in olfactory mucus and VNO. Entirely different chemical mechanisms seem operative with the female-to-female puberty delay chemosignal, 2,5-dimethylpyrazine. This volatile, adrenal-mediated metabolite is also implicated in estrus suppression of mature females. In addition, it has a pronounced and selective effect on chromosomal aberrations in young males.