By Stewart Wolf, Allen K. Murray
The current quantity comprises the edited transcript of a Totts hole Colloquium held might 19-21, 1980 subsidized via the Muscular Dystrophy organization. the purpose of the colloquium used to be to carry into concentration info with regards to cellphone membranes that may give a contribution to realizing the pathogenic mechanism of Duchenne muscular dystrophy. an enormous obstacle to growth in realizing the patho genesis of muscular dystrophy has been the failure, up to now, to spot the elemental genetic illness. Pending the identity of the genetic lesion in Duchenne dystrophy and, in view of scattered yet continual symptoms of a easy membrane disturbance, it appeared useful to discover in open discussion the present nation of information of membrane morphology and chemistry with an eye fixed to attainable leads for additional research. The members, drawn from various disciplines, tried to synthesize and reconcile their findings and to spot the most important parts of lack of knowledge wanting exploration. For the main half they refrained from really good jargon and spoke in a language which may be understood by means of the remainder of the crowd. except supplying a assessment of generally various methods to the research of the composition and behaviour of phone membranes, the discussions introduced jointly present think~g on suggestions and techniques to the learn of the pathogenesis of muscular dystrophy. Already the private contacts made on the colloquium have resulted in new inter-institutional collabora tive investigations.
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Additional info for Composition and Function of Cell Membranes: Application to the Pathophysiology of Muscle Diseases
BRANTON: The only genetic disorder in certain the spectrin is broken down do hemolyse and they do not clear correlation is with a very rare mice due to a lack of spectrin because by proteolysis very rapidly. The mice survive. DR. ENGEL: To what extent can what you have learned of the red cell cytoskeleton be applied to other cell types such as cultured muscle cells. DR. BRANTON: There have been studies with Hela cells and I think also with lymphocytes in which a gentle Triton extraction reveals some kind of a lamellar meshwork underlying the cell membrane and clearly an extensive cytoskeleton internally.
The motion of the lipid in the reconstituted membrane is motionally similar to that of bilayer phospholipid. However, a spectral component referable to immobilized phospholipid in the presence of CPP was detected, equivalent to approximately 8 moles of phospholipid per mole CPP. This small amount of phospholipid appears to be insufficient to constitute a boundary of immobilized phospholipid surrounding the CPP (McIntyre, 1981). Both NMR and EPR studies lead to similar conclusions: 1) To a first approximation the lipid environment in the membrane is homogeneous and typical of a PL bilayer; 2) the CPP in the membrane increases the disorder of the PL:3) there is insufficient PL immobilized to account for a lipid ,"boundary" or "annulus" around the CPP.
Now, i f one extracts the cell to make what are called membrane ghosts of the erythrocyte the lipids and many of the other molecules are removed so that what one PHYLOGENY, STRUCTURE AND COMPOSITION OF CELL MEMBRANES 27 has left is the so-called cytoskeleton or shell. It is the fibrillar anastomosing meshwork that underlies the cell membrane, which as I indicated, is somehow involved in giving the cell its shape. It is also involved in determining the distribution of some of the membrane contours.