Chromosome Transfer Via Cell Fusion

2011 ◽  
pp. 57-67 ◽  
Author(s):  
Marianna Paulis
Keyword(s):  
Cell Fusion ◽  
Chromosome Transfer

scholarly journals Internuclear transfer of genetic information in kar1-1/KAR1 heterokaryons in Saccharomyces cerevisiae.

1981 ◽  
Vol 1 (3) ◽  
pp. 245-253 ◽  
Author(s):  
S K Dutcher
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Fusion ◽  
Genetic Information ◽  
The Other ◽  
Equal Probability ◽  
Chromosome Loss ◽  
Transfer Event ◽  
Chromosome Transfer ◽  
Sequence Of Events ◽  
Donor Nucleus

Heterokaryons of Saccharomyces cerevisiae have been constructed utilizing the kar1-1 mutation, which prevents nuclear fusion during conjugation (J. Conde and G. Fink, Proc. Natl. Acad. Sci. U.S.A. 73:3651-3655, 1976). Each heterokaryon contained two haploid nuclei that were marked on several chromosomes. They segregated haploid progeny (cytoductants), most of which have the nuclear genotype of one or the other of the heterokaryon parents, but they occasionally segregated progeny having a recombinant genotype (exceptional cytoductants). Exceptional cytoductants receive the majority of their genome from one parent (the recipient) and a minority from the other (the donor). Transfer of two markers from the donor nucleus to the recipient is rarely coincident for markers located on different chromosomes but is nearly always coincident for those markers located on the same chromosome, suggesting that whole chromosomes are transferred from the donor nucleus to the recipient. In crosses of kar1-1 X KAR1 parents, either nucleus may act as a recipient or donor with equal probability. Recipient nuclei acquired 9 of the 10 chromosomes examined, with frequencies which were inversely correlated with the size of the chromosome. When a chromosome is acquired by the recipient nucleus, it either replaces its homolog or exists in a disomic condition. Haploid progeny emanating from kar1 X KAR1 crosses are frequently inviable. I tested whether this inviability might be the result of chromosome loss by donor nuclei. Viability of progeny from kar1 X KAR1 heterokaryons was improved when the parental nuclei were diploid to an extent consistent with the hypothesis, and diploid progeny which had become monosomic were recovered from these heterokaryons. The following sequence of events accounts for chromosome transfer in kar1 X KAR1 heterokaryons. After cell fusion, each nucleus in the heterokaryon has a probability of about 0.38 of losing one or more chromosomes. A nucleus sustaining such a loss can become a donor in a chromosome transfer event. If the other nucleus does not sustain a mortal chromosome loss, it can become a recipient in a transfer event. The chance of acquiring a chromosome lost by the donor is greater for smaller chromosomes than for larger ones and is about 0.05 for the average chromosome.

Dissociation of the Hepatic Phenotype from HNF4 and HNF1α Expression

2004 ◽  
Vol 24 (6) ◽  
pp. 595-608 ◽  
Author(s):  
Gary A. Bulla ◽  
David M. Kraus
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Cell Fusion ◽  
Cell Lines ◽  
Tissue Type ◽  
Chromosome Transfer ◽  
Additional Information ◽  
Variant Cell ◽  
Liver Gene

Dedifferentiated cells have served as tools to understand the molecular consequences of the loss of tissue-specific pathways. Here we report the characterization of one of these cell lines, M29, which lacks the liver-enriched HNF4-HNF1α pathway, in order to determine if this class of variant cell lines could provide additional information regarding requirements for tissue-type expression. We report that although the liver-specific α1-antitrypsin (α1AT) gene remains silent despite reactivation of the HNF4/HNF1α pathway in the M29 cells, the frequency of activation of an integrated α1AT-APRT transgene is increased 1000-fold in response to these transcription factors. The human α1AT locus (introduced via chromosome transfer) also remained silent on these cells, despite HNF4 and HNF1α expression. Results from cell fusion experiments suggest that the defect in the M29 cells is recessive. Results suggest that the M29 cells contain a defect that represses liver gene expression despite the presence of the HNF4/HNF1α pathway.

Internuclear transfer of genetic information in kar1-1/KAR1 heterokaryons in Saccharomyces cerevisiae

1981 ◽  
Vol 1 (3) ◽  
pp. 245-253
Author(s):  
S K Dutcher
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Fusion ◽  
Genetic Information ◽  
The Other ◽  
Equal Probability ◽  
Chromosome Loss ◽  
Transfer Event ◽  
Chromosome Transfer ◽  
Sequence Of Events ◽  
Donor Nucleus

Heterokaryons of Saccharomyces cerevisiae have been constructed utilizing the kar1-1 mutation, which prevents nuclear fusion during conjugation (J. Conde and G. Fink, Proc. Natl. Acad. Sci. U.S.A. 73:3651-3655, 1976). Each heterokaryon contained two haploid nuclei that were marked on several chromosomes. They segregated haploid progeny (cytoductants), most of which have the nuclear genotype of one or the other of the heterokaryon parents, but they occasionally segregated progeny having a recombinant genotype (exceptional cytoductants). Exceptional cytoductants receive the majority of their genome from one parent (the recipient) and a minority from the other (the donor). Transfer of two markers from the donor nucleus to the recipient is rarely coincident for markers located on different chromosomes but is nearly always coincident for those markers located on the same chromosome, suggesting that whole chromosomes are transferred from the donor nucleus to the recipient. In crosses of kar1-1 X KAR1 parents, either nucleus may act as a recipient or donor with equal probability. Recipient nuclei acquired 9 of the 10 chromosomes examined, with frequencies which were inversely correlated with the size of the chromosome. When a chromosome is acquired by the recipient nucleus, it either replaces its homolog or exists in a disomic condition. Haploid progeny emanating from kar1 X KAR1 crosses are frequently inviable. I tested whether this inviability might be the result of chromosome loss by donor nuclei. Viability of progeny from kar1 X KAR1 heterokaryons was improved when the parental nuclei were diploid to an extent consistent with the hypothesis, and diploid progeny which had become monosomic were recovered from these heterokaryons. The following sequence of events accounts for chromosome transfer in kar1 X KAR1 heterokaryons. After cell fusion, each nucleus in the heterokaryon has a probability of about 0.38 of losing one or more chromosomes. A nucleus sustaining such a loss can become a donor in a chromosome transfer event. If the other nucleus does not sustain a mortal chromosome loss, it can become a recipient in a transfer event. The chance of acquiring a chromosome lost by the donor is greater for smaller chromosomes than for larger ones and is about 0.05 for the average chromosome.

Cell Fusion is a Potent Inducer of Aneuploidy and Drug Resistance in Tumor Cell/ Normal Cell Hybrids

2013 ◽  
Vol 18 (1 - 2) ◽  
pp. 97-113 ◽  
Author(s):  
Benjamin Berndt ◽  
Kurt S. Zanker ◽  
Thomas Dittmar
Keyword(s):  
Drug Resistance ◽  
Tumor Cell ◽  
Cell Fusion ◽  
Normal Cell ◽  
Potent Inducer ◽  
Cell Hybrids

The Dark Side of Stem Cells: Triggering Cancer Progression by Cell Fusion

2013 ◽  
Vol 13 (5) ◽  
pp. 735-750 ◽  
Author(s):  
T. Dittmar ◽  
C. Nagler ◽  
B. Niggemann ◽  
K.S. Zanker
Keyword(s):  
Stem Cells ◽  
Cell Fusion ◽  
Cancer Progression ◽  
Dark Side
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