| First Author | Kluxen FW | Year | 1988 |
| Journal | Eur J Biochem | Volume | 176 |
| Issue | 1 | Pages | 153-8 |
| PubMed ID | 3138114 | Mgi Jnum | J:9357 |
| Mgi Id | MGI:57818 | Doi | 10.1111/j.1432-1033.1988.tb14262.x |
| Citation | Kluxen FW, et al. (1988) Opposite regulation of the mRNAs for parvalbumin and p19/6.8 in myotonic mouse muscle. Eur J Biochem 176(1):153-8 |
| abstractText | The gene mutation in the mouse, 'arrested development of righting response', adr, causes a defect of chloride conductance of the muscle fibre membrane leading to the symptoms of myotonia [Mehrke, G., Brinkmeier, H. and Jockusch, H. (1988) Muscle & Nerve 11, 440-446]. In fast muscle, the myotonic phenotype is accompanied by a drastic reduction of the Ca2+-binding protein, parvalbumin. Messenger RNA levels in organs of myotonic (ADR) mice were analysed. In fast muscles of the mutant, in-vitro-translatable parvalbumin mRNA was strongly reduced, whereas the mRNA for the slow-muscle-specific protein, p19/6.8, was increased. In contrast, the parvalbumin mRNA in the cerebellum was not affected by the adr mutation. A reduction of the two parvalbumin mRNA species (700 and 1100 nucleotides) in ADR fast muscle and unaltered parvalbumin mRNA levels in mutant cerebella were demonstrated by cDNA/mRNA hybridisation, using a rat parvalbumin cDNA as a probe. The mRNA level for another Ca2+-binding protein, calmodulin, was low in muscle and high in the central nervous system but was unaffected by the mutation. When adr/adr mice were fed a diet containing the membrane-stabilising drug, tocainide, the levels in muscle of the mRNAs for parvalbumin and p19/6.8 were partially normalised. |
