Shiverer peripheral myelin contains P₂

Abstract

Myelin-deficient mutant mice, such as shiverer, can provide information about the normal mechanisms involved in myelination. The shiverer mouse carries a recessive, autosomal mutation¹ resulting in an extreme deficiency in central myelin, and the small amount of myelin present is poorly compacted²; the peripheral myelin, however, appears essentially normal^3,4. As the amount of myelin basic protein (P₁) in both central and peripheral nervous system myelin is extremely low in shiverer^3,5, it is possible that P₁ is essential for the normal formation and compaction of central myelin, but not of peripheral myelin. Some other protein would then be responsible for the formation of compact peripheral myelin in shiverer. Peripheral myelin contains another basic protein, designated P₂, which could be a possible candidate for this role. Kirschner and Ganser, however, using SDS-polyacrylamide gel electrophoresis, reported that P₂, as well as P₁, is absent from shiverer sciatic nerve³. This is an important observation if correct, because it not only excludes the possibility that P₂ is required for compaction but also makes it less likely that the deficiency in P₁ is the primary defect in shiverer. As P₂ in rat and mouse has frequently been confused with another small basic protein (related to P₁) in SDS-polyacrylamide gels⁶, it seemed worthwhile to reassess this aspect of the Kirschner and Ganser observations. Immunohistochemistry and immunoblotting have been used here to show unambiguously that P₂ is present in shiverer peripheral myelin.