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Showing papers by "Carlo M. Croce published in 1979"


Journal ArticleDOI
TL;DR: It is concluded that the genes for human immunoglobulin heavy chains are located on human chromosome 14 in immunoglOBulin-producing human cells.
Abstract: We have studied somatic cell hybrids between P3x63Ag8 mouse myeloma cells deficient in hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) and either human peripheral lymphocytes or human lymphoblastoid or myeloma cells for the production of human immunoglobulin chains and for the expression of enzyme markers assigned to each of the different human chromosomes. Human chromosome 14 was the only human chromosome present in all independent hybrids producing mu, gamma, and alpha human heavy chains. In two of the independent hybrids that produced human heavy chains, human chromosome 14 was the only human chromosome present in the hybrid cells. Loss of human chromosome 14 from these hybrids resulted in the concomitant loss of their ability to produce human immunoglobulin heavy chains. In view of these results, we conclude that the genes for human immunoglobulin heavy chains are located on human chromosome 14 in immunoglobulin-producing human cells.

325 citations


Journal ArticleDOI
TL;DR: Mouse-human hybrid cells were used to study the ability of simian virus 40 to regulate the expression of rRNA genes in vivo, and results indicate that simianirus 40 infection can induce theexpression of otherwise silent r RNA genes.
Abstract: Mouse-human hybrid cells were used to study the ability of simian virus 40 to regulate the expression of rRNA genes in vivo. In these hybrid cells, only the rRNA genes of the dominant species are expressed; the genes for the rRNA of the recessive species are silent. Simian virus 40 infection of these hybrids led to the production of two distinct 28S rRNA species as analyzed by agarose/2.4% polyacrylamide gel electrophoresis. These species were identified as human and mouse rRNAs. This result was confirmed by histochemical studies which indicated that the nucleolus organizer regions of both mouse and human chromosomes were actively synthesizing rRNA in the virus-infected hybrid cells. These results indicate that simian virus 40 infection can induce the expression of otherwise silent rRNA genes.

71 citations


Journal ArticleDOI
TL;DR: The gene coding for human acid alpha-glucosidase is located on human chromosome 17, and 13 independent mouse macrophage x GM54VA hybrid clones were found to express these human enzymes.
Abstract: We have studied somatic cell hybrids between thymidine kinase (EC 2.7.1.75) deficient mouse cells and human diploid fibroblasts for the expression of human acid α-glucosidase (EC 3.2.1.20). A deficiency in this enzyme is associated with the type II glycogenosis or Pompe disease. All 30 somatic cell hybrids selected in hypoxanthine/aminopterin/thymidine medium expressed human acid α-glucosidase and galactokinase (EC 2.7.1.6) and retained human chromosome 17; counterselection of the same hybrids in medium containing 5-bromodeoxyuridine resulted in the growth of hybrids that concordantly lost the expression of human acid α-glucosidase and galactokinase as well as human chromosome 17. Hybrids between thymidine kinase-deficient mouse cells and fibroblasts from a patient with Pompe disease that contained human chromosome 17 were found not to express human acid α-glucosidase. Because we have already shown that hybrids between mouse peritoneal macrophages and GM54VA simian virus 40-transformed human cells selectively retain human chromosome 17 and lose all other human chromosomes, we tested 13 independent mouse macrophage × GM54VA hybrid clones, including two that retained human chromosome 17 and no other human chromosomes, for the expression of human acid α-glucosidase and galactokinase. All 13 hybrid clones were found to express these human enzymes. Thus, we conclude that the gene coding for human acid α-glucosidase is located on human chromosome 17.

40 citations


Journal ArticleDOI
TL;DR: C cultured malignant rat--mouse hybrid cells differentiate normally and become functionally integrated during development and indicate differential gene expression of the introduced xenogeneic chromosomes.
Abstract: Thymidine kinase-deficient OTT6050 mouse teratocarcinoma cells were fused with hypoxanthine phosphoribosyltransferase-deficient Fu5AH rat hepatoma cells by means of inactivated Sendai virus. The resulting hybrid cells, which were selected in hypoxanthine/aminopterin/thymidine medium, retained almost all of the mouse chromosomes and various numbers of rat chromosomes, and showed many chromosomal rearrangements. The hybrid cells, as well as both parental lines, formed tumors after subcutaneous injection into athymic nude mice. Single rat--mouse hybrid cells from a clonally established subline were transplanted into C57BL6/J mouse blastocysts carrying many genetic markers suitable for the detection of hybrid cell-derived tissue contributions. From 144 blastocysts, each of which was injected with a hybrid cell and then surgically transferred to the uterus of a pseudopregnant foster mother, 62 adult mice developed without any visible coat mosaicism. However, three of these mice showed internal hybrid-cell participation in their livers and a limited number of organs of endomesodermal origin. A tumor classifiable as hemangio endothelioma was found in the liver, the only mosaic tissue, of one of the chimeric mice. Nine different rat-specific enzyme variants were detected in the mosaic organs. A considerable number of variations concerning the presence and quantitative activity of the foreign gene products probably resulted from chromosomal segregation, tissue-specific gene activity, or dosage compensation during differentiation in vivo. Our results demonstrate that cultured malignant rat--mouse hybrid cells differentiate normally and become functionally integrated during development. The appearacne in vivo of certain rat-specific gene products that are not found in the hybrid cells under conditions in vitro indicates differential gene expression of the introduced xenogeneic chromosomes.

34 citations


Journal ArticleDOI
TL;DR: Using a chromosome 1 rearrangement, GALE can be assigned to human chromosome 1 by regionally assigning GALE to the pter yields p21 region.
Abstract: The presence of human uridine diphosphate galactose-4-epimerase (GALE) was found to correlate with the presence of chromosome 1 in somatic cell hybrids between man and mouse. The gene for GALE can therefore be assigned to human chromosome 1. Using a chromosome 1 rearrangement, we have been able to regionally assign GALE to the pter yields p21 region.

11 citations


Journal ArticleDOI
TL;DR: A further series of human-mouse hybrids is studied and it is confirmed that the human gene for GALT is located on human chromosome 9.
Abstract: The gene for galactose-1-phosphate uridylyltransferase (GALT) has previously been assigned to human chromosomes 2, 3, and 9. We have studied a further series of human-mouse hybrids and are able to confirm that the human gene for GALT is located on human chromosome 9.

9 citations