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The chromosome complements of human/mouse hybrid cell lines of mouse 3T3-4E and RAG parentage have been analyzed using chromosome banding methods. Three lines that were susceptible to lytic infection with poliovirus contained eleven to seventeen human chromosomes, including chromosome 19. Polio-resistant sublines of these contained no chromosome 19 and showed no other consistent change in the complement of human chromosomes. Human chromosome 19 therefore is essential for polio-sensitivity. Since polio sensitivity was correlated with receptor activity in these lines, we conclude that chromosome 19 carries the structural gene for the poliovirus receptor. Sensitivity to echo-7 and Rhino-1A viruses could not be related to the presence of a specific human chromosome.

Banded karyotypes were prepared for three independent sublines of clone 745A, a Friend virus-induced erythroleukemia cell line originally produced by Dr. C. Friend. Each subline had the same chromosome complement, with a near-diploid number of chromosomes, two-thirds of which appeared normal. The remaining one-third were structurally rearranged marker chromosomes, including eight whose origins could be determined from their banding patterns. A fourth subclone of line 745A, under different selection pressure, showed changes in five marker chromosomes but no changes in the normal chromosomes, suggesting that the markers contained unstable sites, perhaps viral integration sites. Another Friend virus-induced erythroleukemia cell line, FSD-1/F4, developed independently by Dr. W. Ostertag, had a near-diploid number of chromosomes, about one-fourth of which were abnormal chromosomes. The only similarity between these markers and those in subclones of 745A, other than participation of some of the same chromosomes in centric fusion, was the inclusion of the proximal two-thirds of chromosome 15 in one of the markers of each line. This adds to the number of mouse tumor cells or cell lines in which No. 15 is altered or duplicated. In FSD-1/F4 cells there was a striking increase in the size of the secondary constriction of one of the two chromosomes 19, suggesting that the rRNA genes on this chromosome had been amplified.

Nucleolus organizer regions (NORs) of rat chromosomes were stained by the Ag-AS method. The Ag-NORs were found on chromosomes 3, 11 and 12 in the ACI, Wistar Brown and Wistar Lewis inbred strains of rat. The size of the Ag-NOR on each pair of chromosomes varied from strain to strain. Rat-human somatic hybrid cells that retained human and lost some of the rat chromosomes had no Ag-NOR on rat chromosomes 3, 11 or 12. Since NORs can be Ag-stained only if their 18 + 28S rRNA genes are active, the activity of the rat rRNA genes must have been suppressed in the hybrid cells.