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Publication : The genetic analysis of the sensitivity of the CBA/J strain et al

First Author  Biddle F Year  1973
Journal  Mouse News Lett Volume  48
Pages  24 Mgi Jnum  J:46297
Mgi Id  MGI:1202790 Citation  Biddle F, et al. (1973) The genetic analysis of the sensitivity of the CBA/J strain et al. Mouse News Lett 48:24
abstractText  Full text of MNL contribution: UNIVERSITY OF BRITISH COLUMBIA, Division of Medical Genetics, Department of Pediatrics, Vancouyer 8, B.C. Canada. Received; 22nd December 1972 Fred Biddle, Elizabeth March, James R. Miller. Research News: 1. The genetic analysis of the sensitivity of the CBA/J strain and the complete resistance of the SWV strain to the induction of ectrodactyly by acetazolamide is complete. Resistance is dominant or very nearly so; only a few affected CBA.SWV F>l< hybrids have been found while no SWV.CBA F>1< hybrids were recovered. The backcross program using the CBA/J dams was modeled on the study by Dagg et al. (Genetics 53: 1101, 1966) of variations in strain responses to the teratogenic action of 5-fluorouracil. The use of Wright's formula (Genetics 19: 537, 1934) for segregation index gave estimates between 2.63 and 3.44. Therefore, three independent loci control the trait of teratogenic sensitivity to acetazolamide in CBA/J when compared with SWV. This was confirmed by a further backcross breeding program. Also the CBA/J strain phenotype or response frequency was recovered. Embryo transfers successfully demonstrated that the teratogenic environment does exist in the SW strain dams after acetazolamide administration to the dam. The resistance of the SWV strain to acetazolamide is a resistance of the SWV embryo. SWV is also resistant to the induction of ectrodactyly by dichlorphenamide, another carbonic anhydrase inhibitor. Studies with acetazolamide and the C57BL/6J and C57BL/10J strains here and by Dr. Margaret Green at the Jackson Laboratory (personal communication) with other strains have demonstrated a wide variation in ectrodactyly response frequencies and times of action of the teratogen. Therefore, more genetic variability exists in the teratogenic response than that found with the CM/J and SWV strains. (Biddle)
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