Purine Biosynthesis in Chinese Hamster Cell Mutants and Human Fibroblasts Partially Deficient in Adenylosuccinate Lyase

1986 ◽  
pp. 363-369 ◽  
Author(s):  
Paul K. Laikind ◽  
Harry E. Gruber ◽  
Inga Jansen ◽  
Laurie Miller ◽  
Michael Hoffer ◽  
...  
Keyword(s):  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Purine Biosynthesis ◽  
Adenylosuccinate Lyase

DNA-mediated transfer of a human DNA repair gene that controls sister chromatid exchange

1985 ◽  
Vol 5 (4) ◽  
pp. 881-884
Author(s):  
L H Thompson ◽  
K W Brookman ◽  
J L Minkler ◽  
J C Fuscoe ◽  
K A Henning ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Chinese Hamster Cell Line ◽  
Dna Strand ◽  
Repair Defect

The Chinese hamster cell line mutant EM9, which has a reduced ability to repair DNA strand breaks, is noted for its highly elevated frequency of sister chromatid exchange, a property shared with cells from individuals with Bloom's syndrome. The defect in EM9 cells was corrected by fusion hybridization with normal human fibroblasts and by transfection with DNA from hybrid cells. The transformants showed normalization of sister chromatid exchange frequency but incomplete correction of the repair defect in terms of chromosomal aberrations produced by 5-bromo-2'-deoxyuridine.

scholarly journals DNA-mediated transfer of a human DNA repair gene that controls sister chromatid exchange.

1985 ◽  
Vol 5 (4) ◽  
pp. 881-884 ◽  
Author(s):  
L H Thompson ◽  
K W Brookman ◽  
J L Minkler ◽  
J C Fuscoe ◽  
K A Henning ◽  
...  
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Repair Gene ◽  
Dna Repair Gene ◽  
Chinese Hamster Cell Line ◽  
Dna Strand ◽  
Repair Defect

The Chinese hamster cell line mutant EM9, which has a reduced ability to repair DNA strand breaks, is noted for its highly elevated frequency of sister chromatid exchange, a property shared with cells from individuals with Bloom's syndrome. The defect in EM9 cells was corrected by fusion hybridization with normal human fibroblasts and by transfection with DNA from hybrid cells. The transformants showed normalization of sister chromatid exchange frequency but incomplete correction of the repair defect in terms of chromosomal aberrations produced by 5-bromo-2'-deoxyuridine.

2,4-Dichlorophenol and MCPA in a V79 Test

1988 ◽  
Vol 15 (3) ◽  
pp. 245-250
Author(s):  
Geirid Fiskesjö
Keyword(s):  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Test System ◽  
Similar Degree ◽  
Human Beings ◽  
Industrial Chemicals ◽  
Allium Test ◽  
Chinese Hamster Cell Line ◽  
A Cell ◽  
Mutagenic Effects

Two industrial chemicals, 2,4-dichlorophenol and 4-chloro-2-methylphenoxyacetic acid (MCPA), which have no toxic effects on the Chinese hamster cell line V79 alone, were tested for toxicity and mutagenicity in a cell-mediated test, where mixed-function oxidase (MFO) enzymes are active in the metabolism of xenobiotics. For 2,4-dichlorophenol, a dose-dependent toxicity as well as a slight mutagenicity could be shown when oxygenation enzymes were present. A similar degree of toxicity in a plant test system (the Allium test) indicates a similar risk of damage from exposure to dichlorophenol treatments in both these systems. MCPA did not induce any toxic or mutagenic effects at the concentrations tested. These results were not in agreement with previous results in plant material, where MCPA was clearly toxic at relatively low doses. However, since chlorophenols have been found in plants sprayed with phenoxyacetic acids, further investigations should be performed concerning potential risk to human beings.

scholarly journals Glycosylation inhibition reduces cholesterol accumulation in NPC1 protein-deficient cells

2015 ◽  
Vol 112 (48) ◽  
pp. 14876-14881 ◽  
Author(s):  
Jian Li ◽  
Maika S. Deffieu ◽  
Peter L. Lee ◽  
Piyali Saha ◽  
Suzanne R. Pfeffer
Keyword(s):  
Low Density Lipoprotein ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Density Lipoprotein ◽  
Cholesterol Content ◽  
Protein Glycosylation ◽  
Sugar Addition ◽  
Protein Functions ◽  
D Cells ◽  
Niemann Pick

Lysosomes are lined with a glycocalyx that protects the limiting membrane from the action of degradative enzymes. We tested the hypothesis that Niemann-Pick type C 1 (NPC1) protein aids the transfer of low density lipoprotein-derived cholesterol across this glycocalyx. A prediction of this model is that cells will be less dependent upon NPC1 if their glycocalyx is decreased in density. Lysosome cholesterol content was significantly lower after treatment of NPC1-deficient human fibroblasts with benzyl-2-acetamido-2-deoxy-α-D-galactopyranoside, an inhibitor of O-linked glycosylation. Direct biochemical measurement of cholesterol showed that lysosomes purified from NPC1-deficient fibroblasts contained at least 30% less cholesterol when O-linked glycosylation was blocked. As an independent means to modify protein glycosylation, we used Chinese hamster ovary ldl-D cells defective in UDP-Gal/UDP-GalNAc 4-epimerase in which N- and O-linked glycosylation can be controlled. CRISPR generated, NPC1-deficient ldl-D cells supplemented with galactose accumulated more cholesterol than those in which sugar addition was blocked. In the absence of galactose supplementation, NPC1-deficient ldl-D cells also transported more cholesterol from lysosomes to the endoplasmic reticulum, as monitored by an increase in cholesteryl [14C]-oleate levels. These experiments support a model in which NPC1 protein functions to transfer cholesterol past a lysosomal glycocalyx.

Coordinate induction of metallothioneins I and II in rodent cells by UV irradiation

1988 ◽  
Vol 8 (11) ◽  
pp. 4716-4720
Author(s):  
A J Fornace ◽  
H Schalch ◽  
I Alamo
Keyword(s):  
Sequence Analysis ◽  
Uv Irradiation ◽  
Time Course ◽  
Human Fibroblasts ◽  
Chinese Hamster ◽  
Cdna Clones ◽  
X Rays ◽  
General Stress Response ◽  
Rapid Induction ◽  
Kinetics Of

Sequence analysis of Chinese hamster V79 lung fibroblast cDNA clones, which code for UV radiation-inducible transcripts, revealed that many of the clones corresponded to metallothioneins (MTs) I and II. A third cDNA clone, DDIU4, was found also to code for a similar-size UV-inducible transcript which was unrelated to MT by both sequence analysis and kinetics of induction. MTI and MTII RNAs rapidly increased in V79 cells within 1 h after UV irradiation, and maximum induction was seen by 4 h. This rapid induction of MT RNA by UV irradiation was not observed in human fibroblasts. MTI and MTII were coordinately induced in both time course and dose-response experiments, although the induction of MTII, up to 30-fold, was three to four times greater than that of MTI. The induction of MT did not appear to be a general stress response, since no increase occurred after exposure to X rays or H2O2.

Segregation of recessive phenotypes in somatic cell hybrids: role of mitotic recombination, gene inactivation, and chromosome nondisjunction

1981 ◽  
Vol 1 (4) ◽  
pp. 336-346
Author(s):  
C E Campbell ◽  
R G Worton
Keyword(s):  
Somatic Cell ◽  
Chinese Hamster ◽  
Mitotic Recombination ◽  
Chinese Hamster Cell ◽  
Gene Inactivation ◽  
Chromosome Loss ◽  
Resistance Locus ◽  
Chromosome 2 ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids

Somatic cell hybrids heterozygous at the emetine resistance locus (emtr/emt+) or the chromate resistance locus (chrr/chr+) are known to segregate the recessive drug resistance phenotype at high frequency. We have examined mechanisms of segregation in Chinese hamster cell hybrids heterozygous at these two loci, both of which map to the long arm of Chinese hamster chromosome 2. To follow the fate of chromosomal arms through the segregation process, our hybrids were also heterozygous at the mtx (methotrexate resistance) locus on the short arm of chromosome 2 and carried cytogenetically marked chromosomes with either a short-arm deletion (2p-) or a long-arm addition (2q+). Karyotype and phenotype analysis of emetine- or chromate-resistant segregants from such hybrids allowed us to distinguish four potential segregation mechanisms: (i) loss of the emt+- or chr+-bearing chromosome; (ii) mitotic recombination between the centromere and the emt or chr loci, giving rise to homozygous resistant segregants; (iii) inactivation of the emt+ or chr+ alleles; and (iv) loss of the emt+- or chr+-bearing chromosome with duplication of the homologous chromosome carrying the emtr or chrr allele. Of 48 independent segregants examined, only 9 (20%) arose by simple chromosome loss. Two segregants (4%) were consistent with a gene inactivation mechanism, but because of their rarity, other mechanisms such as mutation or submicroscopic deletion could not be excluded. Twenty-one segregants (44%) arose by either mitotic recombination or chromosome loss and duplication; the two mechanisms were not distinguishable in that experiment. Finally, in hybrids allowing these two mechanisms to be distinguished, 15 segregants (31%) arose by chromosome loss and duplication, and none arose by mitotic recombination.

Sign in / Sign up

Export Citation Format

Share Document