Abstract
The taiep mutant rat was first described in a colony of Sprague-Dawley rats at the University of Puebla in 1989, with an autosomal recessive inherited pattern. taiep is an acronym for the progressive neurologic deficits that the rat develops, i.e., t = trembling (3–4 weeks), a = ataxia (at 4 months), i = immobility (5–6 months), e = epilepsy (5–6 months), and p = paresis (7 months onwards). Thus, mutant rats are first identified by a tremor at 3–4 weeks of age that is followed by a progressive neurological worsening (Holmgren et al. 1989; Lunn et al. 1997). The cause of the neurological symptoms is an early failure of normal myelination of the central nervous system (CNS) followed by progressive demyelination of certain CNS tracts (Lunn et al. 1997). We have been exploring the underlying pathophysiology of the mutant and have determined that the myelin defect results from the progressive accumulation of microtubules in oligodendrocytes, the myelin-producing cells of the CNS (Song et al. 1999). Microtubules are the major component of the cytoskeleton of this and many other cells of the body, and microtubule-based transport of protein and mRNA is essential for normal cell function. There is no direct human counterpart of the taiep rat. Nonetheless, providing an understanding of the control of microtubule dynamics in the oligodendrocyte will be highly relevant to our knowledge of the cell biology of the myelinating cell of the CNS. This information is of great relevance to the function of the cell in human myelin disorders and in experimental remyelination. As the taiep rat apparently has a primary disorder in the oligodendrocyte cytoskeleton, it is an ideal model in which to study this process. This information may also be a key to the complete understanding of the mechanism of microtubule assembly/disassembly in many cell types.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
RW Cottingham Jr RM Idury AA Schaffer (1993) ArticleTitleFaster sequential genetic linkage computations. Am J Hum Genet 53 252–263 Occurrence Handle8317490
B Holmgren R Urba-Holmgren L Riboni EC Vega-SaenzdeMiera (1989) ArticleTitleSprague Dawley rat mutant with tremor, ataxia, tonic immobility episodes, epilepsy and paralysis. Lab Anim Sci 39 226–228 Occurrence Handle1:STN:280:BiaB28%2FitFI%3D Occurrence Handle2724922
KF Lunn MK Clayton ID Duncan (1997) ArticleTitleThe temporal progression of the myelination defect in the taiep rat. J Neurocytol 26 267–281 Occurrence Handle1:STN:280:ByiA3srmt1I%3D Occurrence Handle9192292
AA Schaffer (1996) ArticleTitleFaster linkage analysis computations for pedigrees with loops or unused alleles. Hum Hered 46 226–235 Occurrence Handle1:STN:280:BymH3c%2FpsFQ%3D Occurrence Handle8807326
J Song PW Baas ID Duncan (1999) ArticleTitleMicrotubule alterations in cultured taiep rat oligodendrocytes lead to deficits in myelin membrane formation. J Neurocytol 28 671–84 Occurrence Handle1:STN:280:DC%2BD3M%2FhtFWrsw%3D%3D Occurrence Handle10851346
J Song JH Carson E Barbarese FY Li ID Duncan (2003) ArticleTitleAnterograde mRNA transport inhibited in microtubule accumulated oligodendrocytes from the taiep mutant rat. Mol Cell Neurosci . .
Acknowledgements
The authors thank the NHLBI Mammalian Genotyping Service in the Marshfield Clinic, Marshfield, Wisconsin for their help with the genotyping work and Dr. James Weber for reviewing this manuscript. This project was supported by NIH grant NS32361.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Li, FY., Song, J. & Duncan, I.D. Mapping of taiep rat phenotype to rat Chromosome 9 . Mamm Genome 14, 703–705 (2003). https://doi.org/10.1007/s00335-003-2302-z
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1007/s00335-003-2302-z