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Molecular Neurobiology Laboratory, Tsukuba Life Science Center, The Institute of Physical and Chemical Research (RIKEN), 3-1-1 Koyadai, Tsukuba, Ibaraki 305 [N. Y., J. A., K. M.]; Department of Microbiology and Immunology [N. Y.] and 1st Department of Pathology [T. I., H. S.], Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu, Shizuoka 431-31; Department of Pathology, Shizuoka Children's Hospital, 860 Urushiyama, Shizuoka 420 [Y. H.]; Department of Genetics, Research Institute, International Medical Center of Japan, 1-21-1 Toyama-cho, Shinjuku-ku, Tokyo 162 [S. T., K. Y.]; and Department of Molecular Neurobiology, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108 [K. M.], Japan
Zic is a novel zinc finger protein which displays a highly restricted expression pattern in the adult and developing mouse cerebellum and is highly homologous to the recently cloned Drosophila pair-rule gene Opa. To clarify the mechanism for the development of the human cerebellum and its involvement in human nervous system diseases, we have isolated human Zic cDNA and examined its expression by using monoclonal antibody against recombinant Zic protein. The nucleotide sequence of human Zic cDNA is 85% homologous to that of mouse Zic cDNA. Its putative amino acid sequence is highly conserved (>99%) except for substitution of only two amino acid residues. In situ chromosome hybridization localized the human Zic gene to chromosome band 3q24. Human Zic protein was immunohistochemically detected in the nuclei of the cerebellar granule cell lineage from the progenitor cells of the external germinal layer to the postmigrated cells of the internal granular layer. Furthermore, Zic protein was detected in medulloblastoma (26/29 cases), whereas no other tumors examined (over 70 cases including primitive neuroectodermal tumors) expressed this protein. These findings suggest that Zic is a potential biomarker for medulloblastoma as well as the human cerebellar granule cell lineage.
1 This study was supported in part by grants from the Institute of Physical and Chemical Research (RIKEN), Science and Technology Agency, Japanese Ministry of Education, Science, and Culture, and Japan Intractable Disease Foundation.
2 To whom requests for reprints should be addressed.
Received 8/21/95. Accepted 11/ 9/95.
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