Recently we have purified to homogeneity and characterized an interferon-induced human protein (p78 protein) which is the equivalent of the interferon-induced murine Mx protein responsible for a specific antiviral state against influenza virus infection. A cDNA library was constructed using mRNAs from interferon-induced human diploid fibroblasts. cDNA clones coding for the human p78 protein were identified and used to determine the chromosomal location of the corresponding gene (termed IFI-78K gene) by hybridization to DNA from a panel of human x rodent somatic cell hybrids. The newly identified gene is located on chromosome 21. This has been confirmed by the observation of a gene dosage effect using chromosome 21 trisomic cells (fibroblasts derived from Down's syndrome patients). Among all interferon-inducible genes mapped so far, the IFI-78K gene is the only one located on chromosome 21, together with the gene for the receptor of type I interferon. Our results also provide further evidence for homology between human chromosome 21 and mouse chromosome 16, since the gene encoding the mouse Mx protein (the presumed mouse homolog protein of human p78 protein) has been assigned to chromosome 16.
We have applied the representational difference analysis (RDA) to isolate genetic markers for a deletion on the rat chromosome RNO5q22-33. This deletion occurred in anchorage independent sublines of a normal rat fibroblast x mouse hepatoma cell hybrid (BS181) (Islam 1989). Normal rat tissue DNA provided the "tester" and the BS181 hybrid DNA the "driver" in the RDA hybridization/selection reactions. Out of twelve RDA derived DNA sequences that were analyzed in detail using a rat X mouse cell hybrid panel for chromosome mapping, nine (75%) were found to represent RNO5 deletions, whereas the other three were new RFLPs mapping to other chromosomes. In two cases, the RDA sequences were also analyzed by fluorescence in situ hybridization (FISH) and found to give distinct signals in the RNOq22-33 region. This result emphasizes teh significance of the previous cytogenetic analysis of this hybrid, which indicated the presence of a gene for the suppression of anchorage independence, Sai 1, in this deletion region. The RDA derived sequences isolated by this work will provide a valuable source of new genetic markers for the further detailed analysis of the Sai 1 deletion region.
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