Showing papers by "Carlo M. Croce published in 1973"
TL;DR: A linkage relationship between human chromosome C-7, SV40 T-antigen gene(s), and SV40 genome(s) integrated in the human transformed cells is indicated.
Abstract: Hybrid cell clones between mouse cells deficient in thymidine kinase (EC 2.7.1.21) and two different human cell lines transformed by simian virus 40 (SV40) and deficient in hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) were examined for SV40 tumor (T) antigen(s). Concordant segregation of the gene(s) for SV40 T antigen and human chromosome C-7 was observed in these hybrids. The human chromosome C-7 which contains the gene(s) for SV40 T antigen is preferentially retained by the majority of the hybrid clones tested. When hybrid clones positive and negative for SV40 T antigen, derived from the fusion of SV40-transformed Lesch-Nyhan fibroblasts with mouse cells, were fused with CV-1 permissive cells, SV40-specific V antigen was observed only in the cultures derived from fusion of the hybrid clones positive for T antigen. This result indicates a linkage relationship between human chromosome C-7, SV40 T-antigen gene(s), and SV40 genome(s) integrated in the human transformed cells.
101 citations
TL;DR: Negative correlation between the human X chromosome and inducibility of the enzyme was clearly established and the human repressor for inducible tyrosine aminotransferase can be assigned to the X chromosome.
Abstract: The inducibility of tyrosine aminotransferase (EC 2.6.1.5) by corticosteroid hormones in rat-human hybrid clones was studied. The presence of human X chromosome activity in the cells was always associated with the suppression of tyrosine aminotransferase inducibility in all the clones examined. Negative correlation between the human X chromosome and inducibility of the enzyme was clearly established. Corticosteroid receptor was present to the same extent in hybrid cell clones that either contained or lost the human X chromosome. The human repressor for inducible tyrosine aminotransferase has a linkage relationship with glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and hypoxanthine-guanine-phosphoribosyltransferase (EC 2.4.2.8) and, therefore, can be assigned to the X chromosome.
54 citations
TL;DR: Fusion of the 1R mouse cell, which lacks activity of hypoxanthine phosphoribosyl transferase, with chick-embryo fibroblasts yielded progeny cells that survived in hyp oxanthine-aminopterin-thymidine selective medium, and electrophoretic analysis revealed the enzyme was of mouse, not chick, origin.
Abstract: Fusion of the 1R mouse cell, which lacks activity of hypoxanthine phosphoribosyl transferase (EC 2.4.2.8), with chick-embryo fibroblasts yielded progeny cells that survived in hypoxanthine-aminopterin-thymidine selective medium. This property and the failure of the progeny to survive in 8-azaguanine indicated that hypoxanthine phosphoribosyl transferase activity was present. Electrophoretic analysis revealed that the enzyme was of mouse, not chick, origin. These observations are consistent with the operation of a regulator gene responsible for the absence of hypoxanthine phosphoribosyl-transferase activity in the 1R cell and its presence in the progeny.
39 citations
TL;DR: The observed reexpression of rat HPRT in hybrid cells derived from H PRT(-) rat cells suggests that a genetic factor from the human cell determined the expression of the rat structural gene for HPRt.
Abstract: Fusion of hypoxanthine phosphoribosyltransferase (HPRT)- rat hepatoma cells with HPRT+ human fibroblasts yielded hybrid clones that grew in HAT selective medium and contained all the rat chromosomes and one to nine human chromosomes. Among the retained chromosomes was the human X chromosome. In all clones backselected in medium containing 8-azaguanine, human X chromosome was absent. Electrophoretic analysis revealed that, without exception, hybrid clones growing in HAT medium had an active HPRT enzyme, either human or rat, or both. When these clones were backselected in 8-azaguanine, they did not show HPRT enzyme activity. Hybrids that contained the human X chromosome also had human glucose-6-phosphate dehydrogenase. The observed reexpression of rat HPRT in hybrid cells derived from HPRT- rat cells suggests that a genetic factor from the human cell determined the expression of the rat structural gene for HPRT.
38 citations
TL;DR: Rescue of SV40 virus after Sendai virus-mediated fusion of transformed mouse or hamster cell lines with permissive monkey cells was strikingly dependent on pH in the range 6.4-8.8, with a maximum at pH 8.4.
Abstract: Rescue of SV40 virus after Sendai virus-mediated fusion of transformed mouse or hamster cell lines with permissive monkey cells was strikingly dependent on pH in the range 6.4-8.8, with a maximum at pH 8.4. The titer of virus recovered at pH 8.4 was 2 logs higher than that at pH 7.6, and 4 logs higher than that at pH 6.4. The pH-sensitive step was neither the number of heterokaryocytes formed, which was essentially the same at pH 7.6 and 8.4, nor the degree of SV40 replication in the monkey cells, which was also unaffected by pH variation in the range 7.2-8.4.
11 citations