A mutation of the circadian timing system (tau gene) in the seasonally breeding Syrian hamster alters the reproductive response to photoperiod change.

Abstract

The tau mutation is a semi-dominant autosomal mutation which, in homozygotes, accelerates the period of the circadian activity cycle by approximately 4 h. In mammals, the circadian system contributes to seasonal photoperiodic time measurement by generating a repeated daily melatonin signal during the hours of darkness. Our earlier studies suggest an altered response to the melatonin signal in tau mutants. This study investigated whether tau and wild-type hamsters exhibit a differential response to photoperiod change. Reproductively active animals were maintained on stimulatory photoperiods of 16 h light (16L) per 24 h (wild-type) or 12L per 20 h (tau) before being exposed to an increase in night-length to 9, 10, 11, 12 or 14 h for 84 cycles. Wild-types exhibited testicular atrophy at 13L:11Dark (13L:11D), with full regression at photoperiods of 12L:12D. Taus exhibited complete regression at photoschedules comprising 10 h darkness or more per 20-h cycle. Plasma prolactin concentrations were decreased following exposure to at least 9 and 10 h darkness in taus and wild-types, respectively. Thus, the tau genotype may exhibit a different critical night-length with respect to both the gonadal and prolactin axes, of approximately 1-2 h shorter than wild-type genotypes. These data support the hypothesis that the circadian tau mutation has altered the basis of photoperiodic time measurement, perhaps by altering the generation and/or interpretation of the melatonin signal.