Limited lifespan in somatic cell hybrids and cybrids

Bunn, Clive L.; Tarrant, G. M.

doi:10.1016/0014-4827(80)90443-7

Cited by 117 publications

(41 citation statements)

References 40 publications

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“…Escape from senescence occurred in every case due to revertant subpopulations which have previously been documented to arise at a rate of 2610 76 in normal6immortal somatic cell hybrids (Bunn and Tarrant, 1980). These were readily visualized as small patches of dividing cells among the arrested cells (not shown).…”

Section: Characterization and Growth Analysis Of Gm8476hff5 Hybridsmentioning

confidence: 76%

“…About two decades ago experiments involving the fusion of normal and immortal human cells showed that the immortalized phenotype is recessive (Bunn and Tarrant, 1980;Muggleton-Harris and DeSimone, 1980;Pereira-Smith and Smith, 1983). Such somatic cell hybrids have a ®nite replicative lifespan, presumably due to factors present in the normal cells that are able to reimpose normal proliferation control.…”

Section: Introductionmentioning

confidence: 99%

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Repression of an alternative mechanism for lengthening of telomeres in somatic cell hybrids

et al. 1999

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Some immortalized cell lines maintain their telomeres in the absence of detectable telomerase activity by an alternative (ALT) mechanism. To study how telomere maintenance is controlled in ALT cells, we have fused an ALT cell line GM847 (SV40 immortalized human skin ®broblasts) with normal ®broblasts or with telomerase positive immortal human cell lines and have examined their proliferative potential and telomere dynamics. The telomeres in ALT cells are characteristically very heterogeneous in length, ranging from very short to very long. The ALT6normal hybrids underwent a rapid reduction in telomeric DNA and entered a senescencelike state. Immortal segregants rapidly reverted to the ALT telomere phenotype. Fusion of ALT cells to telomerase-positive immortal cells in the same immortalization complementation group resulted in hybrids that appeared immortal and also exhibited repression of the ALT telomere phenotype. In these hybrids, which were all telomerase-positive, we observed an initial rapid loss of most long telomeres, followed either by gradual loss of the remaining long telomeres at a rate similar to the rate of telomere shortening in normal telomerase-negative cells, or by maintenance of shortened telomeres. These data indicate the existence of a mechanism of rapid telomere deletion in human cells. They also demonstrate that normal cells and at least some telomerase-positive immortal cells contain repressors of the ALT telomere phenotype.

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Section: Characterization and Growth Analysis Of Gm8476hff5 Hybridsmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Repression of an alternative mechanism for lengthening of telomeres in somatic cell hybrids

et al. 1999

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“…Specifically, they postulated that normal cells, which they assume are programmed to cease dividing, can become transformed to immortality either by losing a regulatory factor (so that in fusion with a normal cell the immortal phenotype is recessive) or by gaining a transformation factor (with the reverse effect of dominance). Later studies by Bunn and Tarrant (1980), who examined the replicative capacity of hybrids produced by fusion between Lesch-Nyhan limited lifespan fibroblasts and HeLa cells, showed that the apparent dominance of HeLa over the limited lifespan phenotype did not, in fact, normally extend to ensuring unlimited lifespan (the fused cells showed a frequency of appearance of indefinitely growing colonies of only about 1 in 2× 105). However, the average lifespan of the hybrids was greater than that of the normal LeschNyhan cells.…”

Section: "Immortalisation" Of Transformed Cellsmentioning

confidence: 99%

“…However, the average lifespan of the hybrids was greater than that of the normal LeschNyhan cells. Bunn and Tarrant (1980) interpreted this last point as evidence against a rigidly programmed cessation of division in the Lesch-Nyhan cells.…”

Section: "Immortalisation" Of Transformed Cellsmentioning

confidence: 99%

Cytogerontology since 1881: A reappraisal of August Weismann and a review of modern progress

1982

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Summary. Cytogerontology, the science of cellular ageing, originated in 1881 with the prediction by August Weismann that the somatic cells of higher animals have limited division potential. Weismann's prediction was derived by considering the role of natural selection in regulating the duration of an organism's life. For various reasons, Weismann's ideas on ageing fell into neglect following his death in 1914, and cytogerontology has only reappeared as a major research area following'the demonstration by Hayflick and Moorhead in the early 1960s that diploid human fibroblasts are restricted to a finite number of divisions in vitro.In this review we give a detailed account of Weismann's theory, and we reveal that his ideas were both more extensive in their scope and more pertinent to current research than is generally recognised. We also appraise the progress which has been made over the past hundred years in investigating the causes of ageing, with particular emphasis being given to (i) the evolution of ageing, and (ii) ageing at the cellular level. We critically assess the current state of knowledge in these areas and recommend a series of points as primary targets for future research.

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“…It has been proposed that cellular senescence is controlled by genes that are activated or have functions at the end of the proliferative lifespan of normal cells. Hybrids between normal cells and tumor cells generally senesce, indicating that immortal cells have lost, mutated or inactivated genes that are required for the program of senescence in normal cells (Bunn and Tarrant, 1980;Pereira-Smith and Smith, 1983;Koi and Barret, 1986). Hybrids between different immortal cell lines sometimes senesce, suggesting different complementing mutations in certain immortal cells (Pereira-Smith and Smith, 1988).…”

Section: Introductionmentioning

confidence: 99%

Identification of a ≦600-kb region on human chromosome 1q42.3 inducing cellular senescence

et al. 2003

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Limited lifespan in somatic cell hybrids and cybrids

Cited by 117 publications

References 40 publications

Repression of an alternative mechanism for lengthening of telomeres in somatic cell hybrids

Repression of an alternative mechanism for lengthening of telomeres in somatic cell hybrids

Cytogerontology since 1881: A reappraisal of August Weismann and a review of modern progress

Identification of a ≦600-kb region on human chromosome 1q42.3 inducing cellular senescence

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