scholarly journals Painting of human chromosomes with probes generated from hybrid cell lines by PCR with Alu and L1 primers

1990 ◽  
Vol 86 (1) ◽  
Author(s):  
C. Lengauer ◽  
H. Riethman ◽  
T. Cremer
1975 ◽  
Vol 17 (3) ◽  
pp. 307-325
Author(s):  
C.J. Marshall

A study has been made of the ribosomal RNA and chromosome constitution of man-mouse hybrid cells. Previous work has shown that no human 28s rRNA is detectable in man-mouse synkaryons. In general human chromosomes are lost from such hybrids. With a recently developed method for distinguishing mouse from human chromosomes, an analysis of various man-mouse hybrid cell lines has been made. This indicates that not all the human chromosomes bearing nucleolar organizers are lost in the hybrid cells and such loss cannot alone explain the absence of human 28s rRNA. An examination of the 28s rRNA synthesized by heterokaryons formed from several different parent cells has revealed that both parental types of 28s rRNA are present in heterokaryons. The control of rRNA synthesis in hybrid cells is discussed.


1973 ◽  
Vol 12 (3) ◽  
pp. 809-830
Author(s):  
P. W. ALLDERDICE ◽  
O. J. MILLER ◽  
P. L. PEARSON ◽  
G. KLEIN ◽  
H. HARRIS

Chromosome studies were done on 18 somatic hybrid cell lines produced by fusing cells of the mouse A 9 line with cells of the human Daudi lymphoblastoid line derived from a patient with Burkitt's lymphoma. The human chromosomes were identified by their quinacrine fluorescent banding patterns. In one hybrid line the human chromosomes were identified also by the centromeric heterochromatin staining technique. Every human chromosome was identified in one or more of the hybrid lines. Some lines were homogeneous in terms of their human chromosome content, while others were quite heterogeneous. Detailed analysis of the A 9 chromosomes in one hybrid line showed very few changes in comparison with the chromosome constitution of the average A 9 cell.


1997 ◽  
Vol 5 (5) ◽  
pp. 307-312 ◽  
Author(s):  
Philippe Coullin ◽  
Brigitte Andréo ◽  
Jean Paul Charlieu ◽  
Jean-Jacques Candelier ◽  
Franck Pellestor

Genome ◽  
1988 ◽  
Vol 30 (2) ◽  
pp. 124-128 ◽  
Author(s):  
Jennifer A. Marshall Graves ◽  
Paula A. Zelesco

Hamster–mouse and hamster–human hybrid cell lines were used to test the hypothesis that a species-specific difference in the timing of centromere separation is the basis for preferential chromosome segregation from interspecific cell hybrids. Colcemid-treated preparations were C-banded to differentiate hamster and mouse chromosomes or G-11 banded to differentiate hamster and human chromosomes. Metaphase spreads showing at least some centromere separation were photographed and the extent of separation, and the species of origin, was determined for each chromosome. There was no evidence that centromere separation of segregant chromosomes was consistently premature or delayed.Key words: chromosome segregation, centromere separation, cell hybrids.


1990 ◽  
Vol 10 (3) ◽  
pp. 1033-1040
Author(s):  
I M Bonapace ◽  
M Sanchez ◽  
S Obici ◽  
A Gallo ◽  
S Garofalo ◽  
...  

Thyroglobulin gene expression was repressed in a rat thyroid cell line transformed with Kirsten murine sarcoma virus. Expression of a dominant selectable marker driven by the thyroglobulin promoter was also inhibited. Somatic cell hybridization of transformed and differentiated thyroid cells resulted in extinction of thyroglobulin gene expression. When transformed cells carrying a dominant selectable marker driven by the thyroglobulin promoter were fused to differentiated cells and expression of this marker was selected, we obtained stable hybrid cell lines expressing both the endogenous and the exogenous thyroglobulin promoters. Although the expression of v-ras remained unchanged compared with expression in the parental transformed cells, transformation was suppressed in the hybrid cell lines. The other thyroid differentiation markers, iodide uptake and thyroid-stimulating hormone-dependent growth, were inhibited in all the hybrids tested. We show that activity of the thyroglobulin promoter correlates with the presence of a thyroid nuclear factor that binds the promoter at position -60 from the transcription start site. Loss of this factor accompanies the extinction of thyroglobulin gene expression in hybrids selected for expression of a non-thyroid-specific promoter.


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