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Summary. The present study examined the magnitude of genetic variation, mode of inheritance and number of loci controlling major genetic differences in hormone-induced ovulation rate in mice. Mice were injected with 5 i.u. PMSG at 28 days of age and 5 i.u. hCG at 30 days, and hormone-induced ovulation rate was determined from counts of oviducal eggs in cumulus the next morning. Six-fold genetic differences in induced ovulation rate were detected amongst strains, ranging from a low mean (± s.e.) value of 8·8 (±0·9) in A/J up to 53·5 (±2·2) in C57BL/6J. The number of ova differed significantly amongst strains and amongst F₁ crosses (P < 0·0001): 70% of the variation in hormone-induced ovulation rate was amongst strains. Of 9 F₁ crosses examined, 4 showed positive heterosis, 3 showed no heterosis and 2 showed negative heterosis for hormone-induced ovulation rate. Analysis of parental, F₁ and F₂ generations revealed that the induced ovulation rate of A/J and C57BL/6J mice differed due to the action of about 3 or 4 loci, and A.SW/SnJ and SJL/J mice differed due to the action of about 2 to 3 loci. Analysis of recombinant inbred strains formed from A/J and C57BL/6J confirmed that these strains differed due to the action of a small number of loci. This study demonstrates the existence of a small number of major genes controlling hormone-induced ovulation rate in young mice.

Keywords: genes; ovulation rate; mice; heterosis

Summary. Major genetic differences in hormone-induced ovulation rate were not explained by strain differences in age at puberty, by maturation and ovulation of follicles by endogenous gonadotrophins, or by differential responses to gonadotrophins at different ages. The major genetic differences in hormone-induced ovulation rate were explained by strain differences in ovarian responsiveness to exogenous gonadotrophins.

Keywords: ovulation rate; mouse; genetic differences

Summary. Selection for litter size (Line SI) and for post-weaning body weight gain (Line G) increased spontaneous ovulation rate in mature females by 69 and 73%, respectively, over that of randomly bred control mice (Line C). Inbreeding from S1 mice with selection for litter size produced highly inbred lines with elevated ovulation rates. Inbreeding from Line C mice produced a 21% divergence among lines, but did not depress the mean ovulation rate. Crosses of these lines revealed little heterosis in ovulation rate. LH receptors were induced by treating females from 22 days of age with diethylstilboestrol for 4 days and FSH for 2 days. The in-vitro binding of ^{1 25}I-labelled hCG per μg DNA decreased 56% in response to selection for litter size and increased 57% in response to selection for body weight gain, indicating high susceptibility of this trait to genetic change. Inbreeding from Line C mice produced a 135% divergence amongst lines, but did not depress the mean LH receptor induction. Body weight had significant effects on ovulation rate and LH receptor induction.

These results show that selection for litter size and for rapid post-weaning body weight gain increases ovulation rate, but we suggest that different mechanisms are involved in these responses.