A lack of telomeric non-reciprocal recombination (TENOR) may account for the premature proliferation blockade of Werner's syndrome fibroblasts.

摘要: Cell lineages survive as long their descendants replicate. In human diploid fibroblasts (HDF) there is a telomere-driven clock that determines the limited replicative life span of cell branches. Werner's syndrome (WF) prematurely limit compared to HDF on account defective RecQ helicase, WRNp. Here, we introduce concept telomeric non-reciprocal recombination (TENOR) and suggest its dysregulation in WF responsible for premature senescence. We postulate TENOR functions at level four-strand replisomes which are specific initiated fused chromosome ends. Consequently, healthy replicatively senescent can undergo one further division mediated by event. Thereby, two daughter cells re-acquires proliferation capacity initiates new proliferating branch from formerly cell. argue unique mechanisms action WRNp support this concept, apply it WF. If stipulated because WRNp, simple model emerges how they become senescent.