Author:
Zühlke Ch.,Schöffl F.,Jockusch H.,Simon D.,Guénet J.-L.
Abstract
SummaryIn the homozygous condition, the mutationadr(arrested development of righting response) of the mouse causes a myotonia and a drastic reduction of the Ca2+-binding protein parvalbumin (PV) in fast muscles. Using a rat PV probe, a mouse cDNA clone was isolated from a λgt11 wild-type fast-muscle library and its nucleotide sequence was determined. The protein coding and the 3′ non-translated regions of the mouse gene show extensive homology with the rat PV gene. The result of Southern blot hybridization is consistent with a single copy gene for parvalbumin. Restriction fragment length polymorphisms (RFLPs) betweenMus musculus domesticus(e.g. C57BL/6) andMus spretus(SPE) were detected with the enzymesEcoRI,PstI, andSstI. The restriction fragment patterns of DNA samples from 65 individual offspring of (C57BL/6 × SPE)F1 × C57BL/6 backcrosses were tested with the PV probe and matched, for linkage detection, to pre-existing patterns established with various RFLP probes on the same samples. A co-distribution of PV-RFLPs withPvt-1 andMlvi-2, which had been localized on chromosome 15, was detected. Thus, the structural gene for PV, designatedPva, maps to chromosome 15 of the mouse whereas theadrmutation shows no linkage with markers on this chromosome. Gene locus homology between chromsome 15 of the mouse and chromosome 22 of man (which carries the human PV gene) is discussed.
Subject
Genetics,General Medicine
Cited by
27 articles.
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