Mapping through somatic cell hybrids and cDNA probes of protein C to chromosome 2, factor X to chromosome 13, and ?1-acid glycoprotein to chromosome 9

1986 ◽  
Vol 74 (1) ◽  
Author(s):  
M. Rocchi ◽  
L. Roncuzzi ◽  
R. Santamaria ◽  
N. Archidiacono ◽  
L. Dente ◽  
...  
1981 ◽  
Vol 1 (4) ◽  
pp. 336-346
Author(s):  
C E Campbell ◽  
R G Worton

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.


1976 ◽  
Vol 16 (1-5) ◽  
pp. 420-421 ◽  
Author(s):  
Meera Khan ◽  
P.L. Pearson ◽  
L.L.L. Wijnen ◽  
B.A. Doppert ◽  
A. Westerveld ◽  
...  

1982 ◽  
Vol 2 (5) ◽  
pp. 564-570
Author(s):  
P M Pitha ◽  
D L Slate ◽  
N B Raj ◽  
F H Ruddle

The human fibroblast interferon gene beta 1 was mapped to human chromosome 9. Sequence homology with a beta 1 cDNA clone was detected in both genomic DNA and induced mRNA of human/mouse or human/hamster somatic cell hybrids containing human chromosome 9, but not in lines lacking this chromosome or those retaining a complex translocation involving chromosomes 9 and 11. Interferon mRNA that did not share sequence homology with the beta 1 cDNA clone was detected in lines containing human chromosomes 2 and 5 but lacking chromosome 9, suggesting the presence of other unlinked interferon sequences in the human genome.


1983 ◽  
Vol 158 (1) ◽  
pp. 9-15 ◽  
Author(s):  
J Groffen ◽  
N Heisterkamp ◽  
J R Stephenson ◽  
A G van Kessel ◽  
A de Klein ◽  
...  

By analysis of a series of somatic cell hybrids derived by fusion of either mouse or Chinese hamster cells with leukocytes from different chronic myelocytic leukemia (CML) patients or from normal donors, we have localized the human oncogene, c-sis, on the q11 to qter segment of chromosome 22 and demonstrated its translocation from chromosome 22 to chromosome 9 (q34) in CML.


1981 ◽  
Vol 59 (4) ◽  
pp. 317-323 ◽  
Author(s):  
Elly Herbschleb-Voogt ◽  
Karl-Heinz Grzeschik ◽  
Peter L. Pearson ◽  
P. Meera Khan

1994 ◽  
Vol 20 (5) ◽  
pp. 391-400 ◽  
Author(s):  
Bruce W. Porterfield ◽  
Olufunmilayo I. Olopade ◽  
Janet D. Rowley ◽  
Manuel O. Diaz

1999 ◽  
Vol 84 (1-2) ◽  
pp. 48-49 ◽  
Author(s):  
S.H. Elsea ◽  
I.B. Clark ◽  
R.C. Juyal ◽  
D.J. Meyer ◽  
D.I. Meyer ◽  
...  

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