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        Animal Breeding: What Does the Future Hold?

        Eisen, E.J. Asian Australasian Association of Animal Productio 2007 Animal Bioscience Vol.20 No.3

        An overview of developments important in the future of animal breeding is discussed. Examples from the application of quantitative genetic principles to selection in chickens and mice are given. Lessons to be learned from these species are that selection for production traits in livestock must also consider selection for reproduction and other fitness-related traits and inbreeding should be minimized. Short-term selection benefits of best linear unbiased predictor methodology must be weighed against long-term risks of increased rate of inbreeding. Different options have been developed to minimize inbreeding rates while maximizing selection response. Development of molecular genetic methods to search for quantitative trait loci provides the opportunity for incorporating marker-assisted selection and introgression as new tools for increasing efficiency of genetic improvement. Theoretical and computer simulation studies indicate that these methods hold great promise once genotyping costs are reduced to make the technology economically feasible. Cloning and transgenesis are not likely to contribute significantly to genetic improvement of livestock production in the near future.

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        Effect of Genotype on Whole-body and Intestinal Metabolic Response to Monensin in Mice

        Fan, Y.K.,Croom, W.J.,Daniel, Linda,McBride, B.W.,Koci, M.,Havenstein, G.B.,Eisen, E.J. Asian Australasian Association of Animal Productio 2006 Animal Bioscience Vol.19 No.4

        Two lines of mice, M16 selected for rapid growth and a randomly selected control ICR as well as their reciprocal crosses were used to study the effects of genotype on whole-body energetics and intestinal responses to monensin. Six mice, eight weeks of age, from each line or reciprocal cross were assigned to one of two treatments, 1) drinking water containing 20 mmol/L monensin dissolved in 0.5% V/V ethanol, and 2) drinking water containing 0.5% V/V ethanol (control) for two weeks. After 11 days (age of 9 weeks and 4 days), whole-body $O_2$ consumption was measured. At the end of two weeks, jejunal $O_2$ consumption, intestinal tissue composition and histomorphometrics as well as the rate and efficiency of glucose absorption were estimated. In comparison with the control, monensin administration in drinking water resulted in less daily water intake (13.4 vs. 15.5 ml/mouse, p<0.01), less protein to DNA ratio of jejunal mucosa (5.41 vs. 6.01 mg/mg, p<0.05), lower villus width (88 vs. $100{\mu}m$, p<0.05), and less jejunal tissue $O_2$ consumption enhancement by alcohol (7.2 vs. 10.5%, p<0.01) in mice. Other than those changes, monensin had little (p>0.05) effect on variables measured in either line of mice or their reciprocal cross. In contrast, the M16 line, selected for rapid growth, as compared to the ICR controls or the reciprocal crosses, had less initial (pre-monensin treatment) whole-body $O_2$ consumption per gram of body weight (1.68 vs. $2.11-2.34{\mu}mol/min{\cdot}g$ BW, p<0.01) as compared to the ICR and reciprocal crosses. In addition, the M16 mice exhibited greater growth (412 vs. 137-210 mg/d, p<0.05), better feed efficiency (41.7 vs. 19.9-29.3 mg gain/g feed, p<0.05), shorter small intestines adjusted for fasted body weight (1.00 vs. 1.22-1.44 cm/g FBW, p<0.05), wider villi (109 vs. $87-93{\mu}m$, p<0.05), more mature height of enterocytes (28.8 vs. $24.4-25.1{\mu}m$, p<0.05) and a lower rate (91 vs. $133-145{\eta}mol\;glucose/min{\cdot}g$ jejunum, p<0.05) and less energetic efficiency (95 vs. $59-72{\eta}mol$ ATP expended/${\eta}mol$ glucose uptake, p<0.05) of glucose absorption compared to the ICR line and the reciprocal cross. Monensin had little (p>0.05) effect on whole-body $O_2$ consumption and jejunal function, whilst selection for rapid growth resulted in an apparent down-regulation of intestinal function. These data suggest that genetic selection for increased growth does not result in concomitant changes in intestinal function. This asynchrony in the selection for production traits and intestinal function may hinder full phenotypic expression of genotypic growth potential.

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