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Published online 16 April 2001. doi:10.1083/jcb.153.2.295
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© The Rockefeller University Press, 0021-9525/2001/4/295/ $5.00
The Journal of Cell Biology, Volume 153, Number 2, April 16, 2001 295-306

Original Article

OSP/Claudin-11 Forms a Complex with a Novel Member of the Tetraspanin Super Family and ß1 Integrin and Regulates Proliferation and Migration of Oligodendrocytes

Seema K. Tiwari-Woodruffa, Alex G. Buznikova, Trung Q. Vua, Paul E. Micevychb,c, Kendall Chena, Harley I. Kornblumc,d, and Jeff M. Bronsteina,d
a Department of Neurology, University of California at Los Angeles School of Medicine, Los Angeles, California 90095
b Department of Neurobiology, University of California at Los Angeles School of Medicine, Los Angeles, California 90095
c Department of Molecular and Medical Pharmacology and Pediatrics, University of California at Los Angeles School of Medicine, Los Angeles, California 90095
d The Brain Research Institute, University of California at Los Angeles School of Medicine, Los Angeles, California 90095

Correspondence to: Jeff M. Bronstein, UCLA School of Medicine, Dept. of Neurology, RNRC 710 Westwood Plaza, Los Angeles, CA 90024. Tel:(310) 794-2158 Fax:(310) 206-9819 E-mail:jbronste{at}ucla.edu.

Oligodendrocyte-specific protein (OSP)/claudin-11 is a major component of central nervous system myelin and forms tight junctions (TJs) within myelin sheaths. TJs are essential for forming a paracellular barrier and have been implicated in the regulation of growth and differentiation via signal transduction pathways. We have identified an OSP/claudin-11–associated protein (OAP)1, using a yeast two-hybrid screen. OAP-1 is a novel member of the tetraspanin superfamily, and it is widely expressed in several cell types, including oligodendrocytes. OAP-1, OSP/claudin-11, and ß1 integrin form a complex as indicated by coimmunoprecipitation and confocal immunocytochemistry. Overexpression of OSP/claudin-11 or OAP-1 induced proliferation in an oligodendrocyte cell line. Anti–OAP-1, anti–OSP/claudin-11, and anti–ß1 integrin antibodies inhibited migration of primary oligodendrocytes, and migration was impaired in OSP/claudin-11–deficient primary oligodendrocytes. These data suggest a role for OSP/claudin-11, OAP-1, and ß1 integrin complex in regulating proliferation and migration of oligodendrocytes, a process essential for normal myelination and repair.

Key Words: tight junctions, myelin, TM4SF, brain, OAP-1


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