Tanaka K, Yamamura K, Fukuchi K, Kawai K, Kumahara Y
Adv Exp Med Biol. 1985;190:341-51. doi: 10.1007/978-1-4684-7853-2_17.
The mechanism of retarded DNA synthesis was investigated by the cell fusion method. The [3H] TdR labeling index of young cells from patients with Werner syndrome (WS cells) X young normal human diploid fibroblast cells (NH cells) was considerably lower than that of NH homodikaryons, but was significantly higher than that of WS homodikaryons. The labeling index of old WS X young NH heterodikaryons was as low as that of WS homodikaryons. The labeling index of WS X HeLa heterodikaryons was the same as that of HeLa homodikaryons. These results indicate that WS cells are somewhat similar to senescent NH cells. The labeling indices in both WS karyoplast X NH heterodikaryons and WS cytoplast X NH cybrids were lower than those in normal karyoplast X NH heterodikaryons and normal cytoplast X NH cybrids, respectively. These results indicate that both nuclear and cytoplasmic environments are involved in the retarded DNA synthesis in WS cells. The most plausible interpretation of all our data is that the retarded DNA synthesis in WS cells could be caused by either the 'senescent factor(s)' or the deficiency of gene product(s) that is necessary for DNA synthesis and could be a secondary consequence of the genetic defect.
采用细胞融合法研究了DNA合成延迟的机制。沃纳综合征患者的年轻细胞（WS细胞）与年轻正常人二倍体成纤维细胞（NH细胞）融合后的[3H]TdR标记指数显著低于NH同核体，但显著高于WS同核体。老龄WS细胞与年轻NH细胞形成的异核体的标记指数与WS同核体一样低。WS细胞与HeLa细胞形成的异核体的标记指数与HeLa同核体相同。这些结果表明，WS细胞在一定程度上类似于衰老的NH细胞。WS细胞核质体与NH细胞形成的异核体以及WS细胞质体与NH细胞形成的胞质杂种的标记指数分别低于正常核质体与NH细胞形成的异核体和正常细胞质体与NH细胞形成的胞质杂种的标记指数。这些结果表明，核环境和细胞质环境均与WS细胞中DNA合成延迟有关。对我们所有数据最合理的解释是，WS细胞中DNA合成延迟可能是由“衰老因子”或DNA合成所必需的基因产物缺乏引起的，并且可能是遗传缺陷的次要后果。
