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Volume 16, Number 24, Issue of December 15, 1996 pp. 7941-7949
Copyright ©1996 Society for Neuroscience

Neural Cell Type-Specific Expression of QKI Proteins Is Altered in quakingviable Mutant Mice

Received Aug. 6, 1996; revised Sept. 24, 1996; accepted Oct. 1, 1996.

Rebecca J. Hardy¹, Carrie L. Loushin², Victor L. Friedrich Jr.¹, Qi Chen², Thomas A. Ebersole², Robert A. Lazzarini¹, and Karen Artzt²

¹ Brookdale Center for Molecular Biology, Mount Sinai Medical Center, New York, New York 10029, and ² Department of Zoology, University of Texas at Austin, Austin, Texas 78712-1064

qkI, a newly cloned gene lying immediately proximal to the deletion in the quakingviable mutation, is transcribed into three messages of 5, 6, and 7 kb. Antibodies raised to the unique carboxy peptides of the resulting QKI proteins reveal that, in the nervous system, all three QKI proteins are expressed strongly in myelin-forming cells and also in astrocytes. Interestingly, individual isoforms show distinct intracellular distributions: QKI-6 and QKI-7 are localized to perikaryal cytoplasm, whereas QKI-5 invariably is restricted to the nucleus, consistent with the predicted role of QKI as an RNA-binding protein. In quakingviable mutants, which display severe dysmyelination, QKI-6 and QKI-7 are absent exclusively from myelin-forming cells. By contrast, QKI-5 is absent only in oligodendrocytes of severely affected tracts. These observations implicate QKI proteins as regulators of myelination and reveal key insights into the mechanisms of dysmyelination in the quakingviable mutant.

Key words: myelination; dysmyelination; nucleus; RNA metabolism; oligodendrocyte; Schwann cell; quaking; STAR proteins

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