Assignment of the gene for cytoplasmic glutamate-oxaloacetate transaminase to mouse chromosome 19 using Chinese hamster x mouse somatic cell hybrids

1980 ◽  
Vol 6 (6) ◽  
pp. 709-717 ◽  
Author(s):  
R. Sch�fer ◽  
J. Doehmer ◽  
I. Rademacher ◽  
K. Willecke
Keyword(s):  
Somatic Cell ◽  
Mouse Chromosome ◽  
Chinese Hamster ◽  
Somatic Cell Hybrids ◽  
Chromosome 19 ◽  
Glutamate Oxaloacetate Transaminase ◽  
Cell Hybrids ◽  
Mouse Somatic Cell

Assignment of the gene for the thrid component of human complement (C3) to chromosome 19 using human mouse somatic cell hybrids

1982 ◽  
Vol 19 (11) ◽  
pp. 1410 ◽  
Author(s):  
A.S. Whitehead ◽  
E. Solomon ◽  
S.P. Chambers ◽  
S. Povey ◽  
W.F. Bodmer
Keyword(s):  
Somatic Cell ◽  
Complement C3 ◽  
Human Complement ◽  
Somatic Cell Hybrids ◽  
Chromosome 19 ◽  
Cell Hybrids ◽  
Mouse Somatic Cell

Chromosome segregation from cell hybrids. III. Segregation is independent of spindle constitution

Genome ◽  
1987 ◽  
Vol 29 (4) ◽  
pp. 528-531 ◽  
Author(s):  
Paula A. Zelesco ◽  
Jennifer A. Marshall Graves
Keyword(s):  
Somatic Cell ◽  
Key Words ◽  
Chromosome Segregation ◽  
Chinese Hamster ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids ◽  
Mouse Somatic Cell ◽  
Β Tubulin

Hamster β-tubulin (detected as a mutant subunit that confers Colcemid resistance) is either not expressed or is underexpressed in Chinese hamster–mouse somatic cell hybrids. This selectivity of tubulin expression suggests that a uniparental mouse spindle might preferentially engage mouse chromosomes and lead to loss of hamster chromosomes. However, the repression of hamster tubulin was found to have no bearing on the direction of chromosome segregation occurring in eight hybrids studied, some of which segregated predominantly mouse and others hamster chromosomes. Key words: chromosome segregation, cell hybrids, spindle, tubulin.

Genetic Analysis with Man–Mouse Somatic Cell Hybrids: Linkage between Human Lactate Dehydrogenase A and B and Peptidase B

Nature ◽  
1970 ◽  
Vol 227 (5255) ◽  
pp. 251-257 ◽  
Author(s):  
F. H. RUDDLE ◽  
V. M. CHAPMAN ◽  
T. R. CHEN ◽  
R. J. KLEBE
Keyword(s):  
Lactate Dehydrogenase ◽  
Genetic Analysis ◽  
Somatic Cell ◽  
Somatic Cell Hybrids ◽  
Cell Hybrids ◽  
Mouse Somatic Cell

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.

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