Characterization of residual hexosaminidase activity in Sandhoff's disease using man-Chinese hamster cell hybrids

1977 ◽  
Vol 39 (3) ◽  
pp. 315-319 ◽  
Author(s):  
H. L. Hoeksema ◽  
A. J. J. Reuser ◽  
A. T. Hoogeveen ◽  
A. Westerveld ◽  
H. Galjaard
Keyword(s):  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Cell Hybrids

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.

Characterization of adriamycin-resistant and radiation-sensitive Chinese hamster cell lines

1992 ◽  
Vol 44 (9) ◽  
pp. 1859-1868 ◽  
Author(s):  
Marguerite A. Sognier ◽  
Zhang Yin ◽  
Richard L. Eberle ◽  
James A. Belli
Keyword(s):  
Cell Lines ◽  
Chinese Hamster ◽  
Chinese Hamster Cell

Characterization of ?-galactosidase isoenzymes in normal and fabry human-Chinese hamster somatic cell hybrids

1977 ◽  
Vol 36 (3) ◽  
pp. 289-297 ◽  
Author(s):  
Mic N. Hamers ◽  
Andries Westerveld ◽  
Meera Khan ◽  
Joseph M. Tager
Keyword(s):  
Somatic Cell ◽  
Chinese Hamster ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids

Construction and characterization of Chinese hamster cell EmtA EmtB double mutants

1983 ◽  
Vol 3 (5) ◽  
pp. 761-772
Author(s):  
S Chang ◽  
J J Wasmuth
Keyword(s):  
Ribosomal Protein ◽  
Cell Lines ◽  
Ribosomal Proteins ◽  
Hybrid Cell ◽  
Polyacrylamide Gel Electrophoresis ◽  
Chinese Hamster ◽  
Chinese Hamster Cell ◽  
Altered Form ◽  
Hybrid Cell Lines

Starting with hybrid cell lines between a Chinese hamster cell EmtA mutant and a Chinese hamster cell EmtB mutant, we have constructed cell lines that are homozygous for mutant alleles at both the emtA locus and the emtB locus, by using a two-step segregation protocol. The EmtA EmtB double mutants are approximately 10-fold more resistant to emetine inhibition than either of the parental mutants. Having both the EmtA mutation and the EmtB mutation expressed in the same cell also results in a level of resistance to cryptopleurine that is significantly higher than a simple additive effect of the two mutations alone. Analysis of ribosomal proteins by two-dimensional polyacrylamide gel electrophoresis demonstrated that a parental hybrid and a first-step segregant, which has lost the wild-type emtA allele, synthesize both a normal and an altered form of ribosomal protein S14, whereas an EmtA EmtB double mutant synthesizes only the altered form of this ribosomal protein. This result confirms that the emtB locus is the structural gene for ribosomal protein S14. Our results also suggest that the products of the emtA and emtB loci interact directly, indicating that the emtA locus, like the emtB locus, encodes a component of the ribosome.

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