Mine Disruption Phenotype

Gene Info

  • Species:Mouse (Mus musculus)
  • GeneID:17136
  • Symbol:Mag
  • Description:myelin-associated glycoprotein
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Gene ID Entry Entry Name Protein Name Type Information
17136 P20917 MAG_MOUSE Myelin-associated glycoprotein (Siglec-4a) DISRUPTION PHENOTYPE Mutant mice appear normal, excepting subtle defects in motor coordination and a slight intention tremor (PubMed:7516497). They have similar numbers of motoneurons as wild-type at birth, but display an important loss of motoneurons during the first week after birth (PubMed:26335717).Five month old mutant mice display a decreased ability to remain on a rotating cylinder (PubMed:15953602). Contrary to wild-type, about 40% of mutant mice have severe episodes of whole-body tremor, both during movement and when resting (PubMed:15953602). The myelination in brain and around peripheral nerves appears grossly normal in young animals, but the periaxonal cytoplasmic collar is often missing in optic nerve (PubMed:7516497, PubMed:9262180, PubMed:9482781, PubMed:9469574). When present, the cytoplasm of the periaxonal collar has generally a disorganized aspect (PubMed:7516497). Mutant mice have an increased percentage of unmyelinated axons in optic nerve (PubMed:9262180, PubMed:9469574). Besides, a small proportion of nerves from mutant mice display redundant myelination, and also rare cases of multiple myelination, where axons are surrounded by two or more compact myelin sheets (PubMed:9469574). Sciatic nerves from over three month old mutant mice show signs of Wallerian degeneration, with redundant myelin, degeneration of myelinated fibers, and an apparent decrease in the diameter of myelinated axons (PubMed:9482781, PubMed:15953602). The distances between neurofilaments in myelinated axons from over 3 month old mice are shorter than normal (PubMed:9482781, PubMed:15953602). With increasing age, mutant mice display progressive axon degeneration in the spinal cord and sciatic nerve, resulting in a decrease of 28% in the number of spinal cord axons after 15 months (PubMed:19158290). Mutant mice display increased motoneuron apoptosis after injury (PubMed:26335717). Likewise, they display strongly increased axon degeneration after treatment with the neurotoxin acrylamide (PubMed:19158290). Mutant mice display much more severe axon loss in response to experimental autoimmune encephalitis (PubMed:19158290). {ECO:0000269|PubMed:15953602, ECO:0000269|PubMed:19158290, ECO:0000269|PubMed:26335717, ECO:0000269|PubMed:7516497, ECO:0000269|PubMed:9262180, ECO:0000269|PubMed:9469574, ECO:0000269|PubMed:9482781}.