Hostname: page-component-77c89778f8-m42fx Total loading time: 0 Render date: 2024-07-17T06:02:41.540Z Has data issue: false hasContentIssue false

The genes for two neuromuscular diseases of the mouse, ‘arrested development of righting response’, adr, and ‘myotonia’, mto, are allelic

Published online by Cambridge University Press:  14 April 2009

Harald Jockusch*
Affiliation:
Developmental Biology Unit, University of Bielefeld, POB 8640, D-4800 Bielefeld 1, F.R.G.
Kordula Bertram
Affiliation:
Developmental Biology Unit, University of Bielefeld, POB 8640, D-4800 Bielefeld 1, F.R.G.
Susanne Schenk
Affiliation:
Developmental Biology Unit, University of Bielefeld, POB 8640, D-4800 Bielefeld 1, F.R.G.
*
* Corresponding author.

Summary

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Two hitherto unmapped recessive autosomal mutations, ‘arrested development of righting response’ (adr) and ‘myotonia’ (mto, now adrmto), were found to be allelic, so that preliminary linkage data on adr and adrmto can now be combined. No linkage was found to the glucose phosphate isomerase (Gpi-1) locus on Chr 7 that marks a region of homology between mouse Chr 7 and human Chr 19, and in man is closely linked to the myotonic dystrophy (DM) gene. The adr gene was expressed on diverse genetic backgrounds including the athymic nude mouse.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1988

References

Aichele, F., Paik, H. & Heller, A. H. (1985). Efficacy of phenytoin, procainamide, and tocainide in murine genetic myotonia. Experimental Neurology 87, 377381.CrossRefGoogle ScholarPubMed
Füchtbauer, E.-M., Reininghaus, J. & Jockusch, H. (1988). Developmental control of the excitability of muscle: transplantation experiments on a myotonic mouse mutant. Proceedings of the National Academy of Sciences (USA) 85, 38803884.CrossRefGoogle ScholarPubMed
Gracy, R. W. & Tilley, B. E. (1975). Phosphoglucose isomerase of human erythrocytes and cardiac tissue. Methods in Enzymology 41, 392400.CrossRefGoogle ScholarPubMed
Heller, A. H., Eicher, E. M., Hallett, M. & Sidman, R. L. (1982). Myotonia, a new inherited muscle disease in mice. Journal of Neuroscience 2, 924933.CrossRefGoogle ScholarPubMed
Jockusch, H. (1982). Motor end-plate disease is expressed in congenitally athymic mice. Experimental Neurology 78, 391396.CrossRefGoogle ScholarPubMed
Jockusch, H. & Bertram, K. (1986). ‘Arrested development of righting response’ (adr) and ‘myotonia’ (mto) are allelic. Mouse News Letter 75, 19.Google Scholar
Mehrke, G., Brinkmeier, H. & Jockusch, H. (1988). The myotonic mouse mutant ADR: electrophysiology of the muscle fiber. Muscle & Nerve 11, 440446.CrossRefGoogle ScholarPubMed
Peters, J. (ed.) (1988). Mouse gene list. Mouse News Letter 80, 1090.Google Scholar
Reininghaus, J., Füchtbauer, E.-M., Bertram, K. & Jockusch, H. (1988). The myotonic mouse mutant ADR: physiological and histochemical properties of muscle. Muscle & Nerve 11, 433439.CrossRefGoogle ScholarPubMed
Rüdel, R. & Lehmann-Horn, F. (1985). Membrane changes in cells from myotonia patients. Physiological Reviews 65, 310356.CrossRefGoogle ScholarPubMed
Sidman, R. C., Cowen, J. S. & Eicher, E. M. (1979). Inherited muscle and nerve diseases in mice: a tabulation with commentary. Annals of the New York Academy of Sciences 317, 497505.Google ScholarPubMed
Watkins, W. J. & Watts, D. C. (1984). Biological features of the new A2G-adr mouse mutant with abnormal muscle function. Laboratory Animals 18, 16.CrossRefGoogle ScholarPubMed
Watts, R. L. (1978). The A2G-adr mouse. In The Biochemistry of Myasthenia Gravis and Muscular Dystrophy (ed. Lunt, G. G. and Marchbanks, R. M.), pp. 309313. London: Academic Press.Google Scholar
Wieringa, B., Brunner, H., Hulsebos, T., Schonk, D. & Ropers, H. H. (1988). Genetic and physical demarcation of the locus for dystrophia myotonica. Advances in Neurology 48, 4770.Google ScholarPubMed