Open AccessOpposite regulation of the mRNAs for parvalbumin and p19/6.8 in myotonic mouse muscle
Author(s) -
KLUXEN FranzWerner,
SCHÖFFL Fritz,
BERCHTOLD Martin W.,
JOCKSUCH Harald
Publication year - 1988
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1988.tb14262.x
Subject(s) - parvalbumin , messenger rna , calmodulin , biology , microbiology and biotechnology , medicine , endocrinology , mutant , myotonia , biochemistry , gene , genetics , enzyme , myotonic dystrophy
The gene mutation in the mouse, ‘arrested development of rightingresponse’, 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 Ca 2+ ‐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 thecerebellum 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 prvalbumin cDNA as a probe. The mRNA level for another Ca 2+ ‐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 inmuscle of the mRNAs for parvalbumin and p19/6.8 were partially normalised.