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Mutations in the myelin proteolipid protein gene alter oligodendrocyte gene expression in jimpy and jimpymsd mice

W B Macklin1, M V Gardinier, Z O Obeso

  • 1Mental Retardation Research Center, Neuropsychiatric Institute, UCLA Medical Center 90024.

Journal of Neurochemistry
|January 1, 1991
PubMed

Insights

The jimpymsd mouse mutation affects myelin proteolipid protein (PLP) gene transcription, reducing PLP and myelin basic protein (MBP) gene expression. This study investigates the molecular basis of dysmyelination in jimpymsd mice.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • The jimpymsd mouse is a model for dysmyelination, characterized by altered myelin proteolipid protein (PLP) and DM20 protein ratios.
  • Previous studies identified a point mutation in exon 6 of the PLP gene in jimpymsd mice, but its functional impact on gene expression was unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the reduced PLP to DM20 protein ratio in jimpymsd mice.
  • To analyze the transcriptional regulation of the PLP gene and other myelin-related genes in jimpymsd mice.

Main Methods:

  • Southern blot analysis to detect alterations in the PLP gene regulatory regions.
  • S1 nuclease analysis to quantify PLP and DM20 mRNA ratios.
  • Gene sequencing to identify mutations in the PLP gene.
  • Analysis of gene transcription rates for PLP, myelin basic protein (MBP), and glycerol phosphate dehydrogenase (GPDH).

Main Results:

  • No alterations were observed in the upstream regulatory regions of the PLP gene in jimpymsd mice.
  • PLP mRNA was consistently elevated above DM20 mRNA in both normal and jimpymsd mice.
  • Transcription rates of both PLP and MBP genes were significantly reduced in jimpymsd mice after 10 days of age, while GPDH transcription remained normal.

Conclusions:

  • The jimpymsd mutation leads to a significant decrease in the transcription rate of the PLP gene and MBP gene.
  • The observed reduction in myelin gene expression, rather than altered mRNA splicing, is likely responsible for the dysmyelination phenotype in jimpymsd mice.
  • The mutation affects the expression of multiple myelin genes, suggesting a broader impact on oligodendrocyte function.

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