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The genetic control of red cell glutathione deficiencies in Finnish Landrace and Tasmanian Merino sheep and in crosses between these breeds

Published online by Cambridge University Press:  27 March 2009

Elizabeth M. Tucker ,
L. Kilgour  and
J. D. Young
L. Kilgour
Affiliation:
A.R.C. Institute of Animal Physiology, Babraham, Cambridge CB2 4AT
J. D. Young
Affiliation:
A.R.C. Institute of Animal Physiology, Babraham, Cambridge CB2 4AT
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Summary

Finnish Landrace sheep with low red cell GSH concentrations resulting from a defective transport system for certain arnino acids were crossed with Tasmanian Merino sheep with a red cell GSH deficiency due to impaired activity of the enzyme γ-glutamyl cysteine synthetase. Inheritance data showed that the two types of GSH deficiency were under independent genetic control. In the Finnish Landrace breed, the gene coding for the transport defect (Trn) was inherited as an autosomal recessive and sheep homozygous for this gene had high red cell concentrations of lysine and ornithine (Ly ×) as well as low levels of GSH. In the Tasmanian Merino breed the GSH deficiency behaved as if controlled by an autosomal dominant gene (GSHL). Backcross breeding experiments resulted in lambs which had inherited both types of GSH deficiency. Evidence suggested that such ‘double low’ GSH lambs had an impaired viability. In Tasmanian Merinos the GSH deficiency was established prior to birth. Newborn Finnish Landrace lambs were clearly separable into two types on the basis of their red cell lysine and ornithine content but not on their GSH concentrations.

Type
Research Article
Information
The Journal of Agricultural Science , Volume 87 , Issue 2 , October 1976 , pp. 315 - 323
Copyright
Copyright © Cambridge University Press 1976

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