In a flock of highly prolific Romney ewes obtained from industry flocks, one ewe (A281), with a production record of 33 lambs born in 11 lambings, produced a number of female descendants with high ovulation rates. The mode of inheritance of this trait was determined in a series of four progeny tests of male descendants of this ewe. The first progeny test produced strong evidence for a new major gene affecting ovulation rate in this family line; this finding was supported by two subsequent progeny tests. The fourth progeny test was designed to test the hypothesis that this gene is carried on the X chromosome. The results showed that six sons of a carrier ram did not inherit the gene, but it was passed on to three of his five maternal grandsons. This finding, together with evidence of genetic segregation in the progeny of carrier females, demonstrates for the first time the presence of a major gene for prolificacy specifically located on the X chromosome. The effect of the gene is to increase ovulation rate by about one additional egg per ewe.

Ewes heterozygous (I+) for the Inverdale prolificacy gene (FecXI) located on the X chromosome have ovulation rates about 1.0 units higher than noncarriers. The purpose of this study was to examine the reproductive performance of ewes that were either heterozygous or homozygous (II) carriers of the Inverdale gene. Carrier rams (I) were mated with heterozygous ewes (I+) to produce females, half of which were expected to be I+ and half II. The 59 female progeny were examined by laparoscopy at 8 mo or 1.5 yr of age; 48% were found to have nonfunctional "streak" ovaries, which were about one eighth the volume of normal ovaries and showed no sign of follicular activity. There were four examples of full sib pairs where within each pair one had normal ovaries and the other had streak ovaries. Since these streak ovaries have not been observed in ewes known to be I+ or noncarriers (++), it is concluded that this condition is associated with animals homozygous for the Inverdale gene.

A series of six studies were carried out in red deer stags to test hypotheses concerning the importance of steroid control of velvet antler growth and to investigate mechanisms by which these hormones exert their effects. Medroxyprogesterone acetate (MPA) an LH inhibitor administered to stags during hard antler caused premature antler casting, reduced subsequent antler weight and caused a reduction in the LH and testosterone responses to GnRH. In two separate studies blockade of testosterone receptors with cyproterone acetate (CPA) administered to stags, either during early velvet antler growth or during the hard antler stage, significantly reduced LH and testosterone responses to GnRH. In both studies antler length, but not weight, was increased by CPA treatment. In another study testosterone implants were used to prevent the gradual decline in plasma testosterone levels normally observed during winter. Implants were removed 3 weeks before the anticipated date of antler casting. The implants significantly increased plasma testosterone levels and subsequent antler growth (expressed as a proportional increase compared with the previous year) compared with untreated controls. To determine whether the annual cycle of plasma testosterone response following GnRH stimulation was due simply to a lack of LH stimulation, ovine LH was injected on six occasions at defined stages of the antler cycle to red deer stags and the testosterone response measured. The testosterone responses were low at antler casting and during velvet antler growth compared with antler cleaning and peak rut. It appears low testosterone levels are due, in part, to a loss of responsiveness by the testes to LH as well as a low level of secretion of LH during the antler growing season. Finally synthetic ACTH was injected at the same defined stages of antler growth as in the previous study to determine whether cortisol and adrenal androgen production altered with the stage of the antler cycle. No significant differences were found in the dehydroepiandrosterone (DHEA) response, but cortisol responses were higher from late velvet antler growth to peak rut, compared with the times of antler casting and early velvet growth. Overall it was concluded that velvet antler growth can occur without testosterone stimulation during the period of velvet growth, but the data reinforce the concept that the timing of antler growth is linked to the annual cycle of testosterone.

No abstract

We have investigated the possibility that IGF-1 may play a role in the regulation of antler development. Plasma IGF-1 concentrations were measured throughout the first period of development of the pedicle and first antler of red deer (Cervus elaphus) to determine whether a relationship existed between growth of antler cartilage (velvet antler) and IGF-1. We report that plasma levels of IGF-1 are significantly elevated during the velvet antler growing phase relative to the other phases of pedicle and first antler development and a strong positive correlation exists between antler growth rate and circulating concentrations of IGF-1. As IGF-1 has been demonstrated to influence cartilage growth, we suggest that IGF-1 is a candidate as an antler stimulating hormone.