Biomedical subjects
G Coulton
Publications and source records attributed to G Coulton.
Isoforms of myosin in growing muscles of ky (kyphoscoliotic) mice.
Kyphoscoliotic (ky) mice are spontaneous mutants of the BDL strain whose postural muscles atrophy during post-natal growth, resulting in extensive kyphoscoliosis in adult animals. At 21 days of age, the seven muscles examined were already well differentiated into fast, slow and mixed type on the basis of the proportions of their native myosin isoforms or their subunits. During post-natal growth, from 21 to 120 days of age, the normal pattern of myosin maturation was essentially respected by the ky mutation: fast muscles became faster, slow muscles became slower and mixed muscles specialized in both directions. However, the post-natal increases of myosin heavy chain 2B and fast myosin light chain LC3f were depressed in ky muscles, whilst there was novel expression of slow myosin light chains, LC1s and LC2s in muscles which normally did not express them. Intermediate native myosin IM was absent in adult ky soleus, but it increased in adult ky tibialis anterior. We conclude that the ky mutation depresses the normal post-natal transition towards faster muscles and results in adult muscles whose myosin isoforms are generally shifted in a fast-to-slow direction.
The cysteine-rich and C-terminal domains of dystrophin are not required for normal costameric localization in the mouse.
Dystrophin has a modular structure and is believed to be critical for muscle cell cytoarchitecture by linking the cytoskeleton to the extracellular matrix. The N-terminus binds to actin and two domains at the C-terminus, the cysteine-rich and C-terminal domains, are associated with the sarcolemma indirectly via the dystroglycan complex. We have generated a mutation in mouse embryonic stem (ES) cells which serves to delete the cysteine-rich and C-terminal domains to address directly their role. We show that these two domains are not necessary for normal costameric organization at the sarcolemma in myotubes derived from the mutant cell line. Furthermore sarcolemmal localization is also apparent in mouse chimaeric muscle in vivo.
In situ hybridization comes of age.
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In situ hybridisation of a Y chromosome-specific probe to male myoblasts after implantation into female skeletal muscle.
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Molecular and genetic mapping of the mouse mdx locus.
mdx is an X-linked muscular dystrophy mutant of the mouse and a putative homolog of the human X-linked muscular dystrophy locus--Duchenne muscular dystrophy (DMD). Utilizing a C57BL/10/Mus Spretus interspecific cross in which the mdx mutation was segregating, we have constructed a detailed genetic map around the mdx locus on the mouse X chromosome. We were unable to detect recombinants between mdx and exonic probes derived from the human DMD gene. These genetic data support the contention from biochemical studies (E.P. Hoffman, R. H. Brown, and L. M. Kunkel, 1987, Cell 51: 919-928) that DMD and mdx are homologous genes.