Genetics of Human-Mouse Somatic Cell Hybrids: Linkage of Human Genes for Lactate Dehydrogenase-
            <i>A</i>
            and Esterase-A
            <sub>4</sub>

Shows, Thomas B.

doi:10.1073/pnas.69.2.348

Cited by 88 publications

(16 citation statements)

References 33 publications

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“…In these hybrids AK1 was always found to be lost (2,19). Also in man-Chinese hamster hybrids (Tables 1 and 2) chromosome 9 appears to be lost more frequently than most of the other chromosomes.…”

Section: Discussionmentioning

confidence: 94%

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Westerveld¹,

Jongsma²,

Khan³

et al. 1976

Proc. Natl. Acad. Sci. U.S.A.

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In man-Chinese hamster somatic cell hybrids the segregation patterns of the loci for 25 human enzyme markers and human chromosomes were studied. The results provide evidence for the localization of the gene for adenylate kinase-1 (AKI) on chromosome 9. Since the loci for the ABO blood group (ABO), nail-patella syndrome (Np), and AK1 are known to be linked in man, the ABO.Np:AKj linkage group may be assigned to chromosome 9.

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Section: Discussionmentioning

confidence: 94%

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Westerveld¹,

Jongsma²,

Khan³

et al. 1976

Proc. Natl. Acad. Sci. U.S.A.

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“…Interspecific somatic ccU hybrids have been useful for the study of gone linkage, the control of gene expression, and the rescue of infectious virus from nonproducer, transformed cells (see, for example, Davidson, 1971 ;Kao and Puck, 1970;Kit ct al., 1970;Shows, 1972). Recently, hybrid cells have also been used to investigate genetic control of mitochondrial cnzyms.…”

Section: Discussionmentioning

confidence: 99%

“…The human-mouse (WIL-8) somatic hybrid cell line was obtained through the courtesy of T. B. Shows, Roswell Park Memorial Institute, Buffalo, N. Y. WIL-8 cells possess a modal chromosome number of about 100, with 12-18 human chromosomes including the human thymidine kinase (El7) and the hypoxanthine-guanine phosphoribosyl transferase (X) chromosomes (Shows, 1972). Cassingena et al, 1971; clone 1 (BUI00) and CV-I cells Kit et al, 1970 HeLaS3 dT kinase-positive human cervical carcinoma cells Gey et al, 1952 Cell lines were grown in 8-ounce prescription bottles in Eagle's minimal essential medium (Auto Pow; Flow Laboratories, Inc., Rockville, Md.)…”

Section: Cell Linesmentioning

confidence: 99%

“…Experiments with the mK.CV III clone 1 monkey-mouse and with the WIL-8 human-mouse cells have shown that these hybrid cell lines, respectively, fail to express the genes governing the synthesis of monkey interferon and human adenylate kinase (Cassingena et al, 1971 ;Shows, 1972). However, mK.…”

mentioning

confidence: 99%

“…However, mK. CV 111 cells do express monkey cytosol dT kinase and monkey deoxycytidylate deaminase, and WIL-8 cells express the following human enzymes: thymidine kinase, lactate dehydrogenase-A, esterase-A4, lactate dehydrogenase-B, glucose 6-phosphate dehydrogenase, cytosol NAD-dependent malate dehydrogenase, cytosol NADP-dependent malic enzyme, phosphoglucomutase, phosphohexose isomerase, supernatant glutamic-oxalacetic transaminase, peptidases A, B, and C, and indophenol oxidase (Kit et al, 1970;Shows, 1972). It can be concluded, tentatively, that the genetic determinant for mitochondrial-specific dT kinase is on a different linkage group from that controlling the synthesis of the primate enzymes indicated above and found in the monkey-mouse and human-mouse hybrid cells.…”

mentioning

confidence: 99%

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Genetic Control of Mitochondrial Thymidine Kinase in Human-Mouse and Monkey-Mouse Somatic Cell Hybrids

Kit

Leung

1974

The Journal of Cell Biology

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Distinctive thymidine (dT) kinase molecular forms are present in mouse, human, and monkey mitochondria. Disk polyacrylamide gel electrophoresis (disk PAGE) analyses have shown that the mitoc.hondrial-specific dT kinases differ from cytosol dT kinases in relative electrophoretic mobilities (Rm). Furthermore, the mouse mitochondrial dT kinase differs in Rm value from primate mitochondrial dT kinases. The mouse and primate cytosol dT kinases can also be distinguished.Disk PAGE analyses have been carried out on the cytosol and mitochondrial dT kinases of human-mouse (WIL-8) and monkey-mouse (mK.CV IH) somatic cell hybrids in order to learn whether the mitochondria of the hybrid cells contained murine mitochondrial-specific, primate mitochondrial-specific, or both dT kinases. WIL-8 cells were derived from cytosol dT kinase-negative, mitochondrial dT kinase-po sitive mouse fibro blasts and from cytosol dT kinase-positive, mitochondrial dT kinase-positive human embryonic lung cells; they contained mostly mouse chromosomes and a few human chromosomes, including the determinant for human cytosol dT kinase. The mK.CV ~H cells were derived from cytosol dT kinase-negative, mitochondrial dT kinase-positive mouse kidney cells and from cytosol dT kinase-positive, mitochondrial dT kinase-positive monkey kidney ceils; they contained mostly mouse chromosomes and a few monkey chromosomes, including the determinant for monkey cytosol dT kinase. Disk PAGE analyses demonstrated that the mitochondria of human-mouse and monkey-mouse somatic cell hybrids contained the mouse-specific mitochondrial dT kinase but not the human-or monkey-specific mitochondrial dT kinase. These findings suggest that primate cytosol and mitochondrial thym idine kinase genes are coded on different chromosomes.

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Genetic heterogeneity of I‐cell disease is demonstrated by complementation of lysosomal enzyme processing mutants

Shows¹,

Mueller²,

Honey³

et al. 1982

Am. J. Med. Genet.

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I-cell disease (mucolipidosis II) is a fatal childhood disorder affecting the expression of multiple lysosomal acid hydrolases. The disorder is characterized by clinical and biochemical heterogeneity which may reflect different mutants with a similar phenotype. Genetic complementation studies demonstrating genetic heterogeneity within this disorder are described utilizing cultured fibroblasts from 11 different patients. Fibroblasts from I-cell disease (ICD) and from five different lysosomal storage diseases with single structural gene enzyme deficiencies were fused in different combinations, and fractions enriched for multinucleated heterokaryons were isolated and tested for acid hydrolase activity and electrophoretic mobility. In fusions of ICD fibroblasts and various single lysosomal enzyme-deficient fibroblasts, the activity of the deficient enzyme and of the other ICD hydrolases were restored, demonstrating that ICD is not a lysosomal enzyme structural gene defect and that the ICD defect, and not just the single enzyme deficiency, is corrected. In fusions involving only I-cell fibroblasts, at least two complementation groups were identified by the recovery of activities of all lysosomal enzymes tested in heterokaryons. These results demonstrate the existence of genetic heterogeneity within the disorder and suggest that different mutations can result in the I-cell clinical and biochemical phenotype. The data support an altered post-translational processing of lysosomal enzymes as the cause of ICD and suggest that at least two genes participate in this pathway.

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Genetics of Human-Mouse Somatic Cell Hybrids: Linkage of Human Genes for Lactate Dehydrogenase- A and Esterase-A ₄

Cited by 88 publications

References 33 publications

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Genetic Control of Mitochondrial Thymidine Kinase in Human-Mouse and Monkey-Mouse Somatic Cell Hybrids

Genetic heterogeneity of I‐cell disease is demonstrated by complementation of lysosomal enzyme processing mutants

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Genetics of Human-Mouse Somatic Cell Hybrids: Linkage of Human Genes for Lactate Dehydrogenase- A and Esterase-A 4

Cited by 88 publications

References 33 publications

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Assignment of the AK1:Np:ABO linkage group to human chromosome 9.

Genetic Control of Mitochondrial Thymidine Kinase in Human-Mouse and Monkey-Mouse Somatic Cell Hybrids

Genetic heterogeneity of I‐cell disease is demonstrated by complementation of lysosomal enzyme processing mutants

Contact Info

Product

Resources

About

Genetics of Human-Mouse Somatic Cell Hybrids: Linkage of Human Genes for Lactate Dehydrogenase- A and Esterase-A ₄