Cell Fusion Studies in the Werner Syndrome
Werner syndrome (WS) is an autosomal recessive hereditary disease characterized by a reduced lifespan and with symptoms of premature senility (Epstein et al. 1966). Skin fibroblast cells from patients with Werner syndrome (WS cells) have a greatly reduced lifespan in vitro and showed marked retarded DNA synthesis even at early ages in culture (Goldstein, 1969; Martin et al., 1970; Danes, 1971; Fujiwara et al., 1977). One approach for the study of senescense of WS cells in vitro is to introduce gene product(s) or a gene itself and to observe changes in DNA synthesis. Norwood et al. (1974, 1975, 1979) demonstrated that DNA synthesis of senescent fibroblasts could be stimulated when these cells were fused with HeLa cells. On the other hand, when these cells were fused with young fibroblasts, no recovery of DNA synthesis was observed. They therefore suggested that the senescent cells have a ‘senescent factor(s)’ that inhibits their DNA synthesis. We also applied cell hybridization techniques in order to define the genetic defect of WS cells. In this article we will discuss the mechanism of aging in WS in comparison with senescent cells.
KeywordsHeLa Cell Label Index Pulse Period Senescent Cell Werner Syndrome
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