The myelin and lymphocyte gene (Mal) encodes a tetraspan raft-associated 
proteolipid predominantly expressed by oligodendrocytes and Schwann 
cells. MAL protein is also involved in the apical delivery of 
fusiform vesicles in urothelial umbrella cells, and is required for the binding and activity of Clostridium perfringens e-Toxin which causes selective death of mature oligodendrocytes and central nervous system demyelination.
These mice carry a targeted knockout of the mouse Mal gene. LacZ/neo 
was inserted after the third codon in exon 1, and replaces the remainder
 of exon 1. Northern blot indicates a lack of full-length transcript in 
homozygotes, but presence of a lacZ-containing transcript in homozygotes
 and heterozygotes. Absence of wild-type protein has been demonstrated by immunohistochemical assay of sciatic nerves and brain from mutants. 
Homozygous knock-out of Mal results in cytoplasmic inclusions within 
compact myelin, paranodal loops that are everted away from the axon and 
disorganized transverse bands at the paranode-axon interface in the 
adult CNS. These structural changes are accompanied by a marked 
reduction of CASPR, Neurofascin 155 (NAFASC; NF155) and the potassium channel 
Kv1.2 (KCNA2), while nodal clusters of sodium channels are unaltered. Initial 
formation of paranodal regions appears normal, but abnormalities become
 detectable when MAL is starting to be expressed. Biochemical analysis 
has revealed reduced MAG, MBP and NF155 protein levels in myelin and 
myelin-derived rafts. Results demonstrate a critical role for MAL in
 the maintenance of CNS paranodes, likely by controlling the trafficking
 and/or sorting of NF155 and other membrane components in 
oligodendrocytes.

These mal KO mice carry a knock-out allele of the mouse Mal (myelin and lymphocyte protein, T cell differentiation protein) gene, useful in studies of axon-glia interactions in the central nervous system. A lacZ/neo reporter replaces a portion of exon 1.

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