To evaluate the genetic relationship within and between wood and plains bison of Elk Island National Park, genomic DNA samples were screened for restriction fragment length polymorphisms (RFLP) with cDNA probes for growth hormone, growth hormone releasing factor, somatostatin, and insulin-like growth factor-1. Of the 28 fragments identified, two revealed RFLPs, both of which were associated with the growth hormone releasing factor locus. The observed frequencies of the polymorphic sites did not differ from a Hardy–Weinberg distribution in either population, which is indicative of random mating populations. The contingency χ2 tests for homogeneity indicate that the fragment frequencies of the polymorphic restriction sites differ significantly (P = 0.00) between the wood and plains bison. The number of net nucleotide substitutions between the two populations was 0.0007, indicative of a recent divergence. Conversion of the bison nucleotide divergence results in a relative protein divergence of 0.007 to 0.018. This converted divergence corresponds closely to the divergence reported for other geographically isolated populations; thus, this preliminary analysis suggests the bison have at least reached the stage of geographic isolation in their evolutionary divergence.

Blood samples were taken from 19 double-muscled (DM) and 20 normal (N) bull calves at the ages of 1.5, 2, 2.5, 3, 3.5, 4, 5.5, 6.5 and 9 mo to compare the plasma concentrations of growth hormone and insulin in DM with those in N bull calves and to relate these to differences in growth rate between the two breed groups. Double-muscled bull calves were lighter (P less than .0001) than N calves at all ages and had lower (P less than .001) preweaning and postweaning rates of gain. Double-muscled bull calves had lower (P less than .01) mean growth hormone concentration than N calves. Mean growth hormone concentration was correlated positively with body weight and preweaning rate of gain. The effect of age on growth hormone concentration was linear (P less than .05); however, mean growth hormone concentration fluctuated between ages 1.5 to 4.5 mo but stabilized after 5.5 mo of age in both breed groups. Mean insulin concentration was lower (P less than .01) in DM than in N bull calves. The effect of age on insulin concentration was both linear and quadratic (P less than .0001). Mean insulin concentration generally was constant in both breed groups, at around .75 ng/ml, from 1.5 to 6.5 mo of age but rose sharply to around 1.67 ng/ml after weaning when the bulls were put on a high-energy diet.

Restriction site analysis revealed a variant growth hormone gene haplotype fixed within growthselected mice (High line-3; HL-3) exhibiting growth rates 1-5 times greater than those of unselected Foundation population (FP-3) mice. Relative to the FP-3 haplotype, the HL-3 haplotype exhibited restriction fragment length polymorphisms for each of seven different restriction enzymes. Three of the polymorphic sites lie within 11 kb of the 5' end of the structural gene; a fourth polymorphism exists within the structural gene. The HL-3 haplotype was also fixed within an additional three growth-selected lines (including a replicate of HL-3). This identification of an association, between the natural variant of a growth regulating gene and a growth-related phenotype, is the prototype of experiments that could lead to the isolation of variant genes which enhance livestock production characters.

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Two specific oligonucleotide probes complementary to different regions of human sex steroid-binding protein (SBP) cDNA were used to study the levels of hepatic monkey SBP mRNA during different hormonal states. In females the SBP mRNA level was higher than in males and paralleled the serum SBP level. After castration, the SBP concentration increased in the serum but was reduced after testosterone treatment. In contrast, the hepatic SBP mRNA level decreased after castration and was restored by testosterone treatment. These results suggest a high homology of the nucleotide sequence between human and monkey SBP mRNAs. The changes in liver SBP mRNA levels may explain the sex difference in plasma SBP concentrations, but mechanisms other than the regulation of transcription may regulate the plasma concentration in monkeys.