Werner syndrome (WS) is a rargon autosomal recessive dis coordinate characterized by premature agedness (von Kobe, et al., 2003). It is named subsequently the German physician Carl W. Otto Werner (1879-1936), who offset base described the syndrome as part of his doctoral thesis in 1904. WS is caused by mutations in the RecQ family of helicase which be encoded by chromosome 8p by the WRN divisor (Moser, et al., 1999). The mutations truncate the WRN protein with a loss of up to 1256 amino group dosages. In other words, WS is caused by a helicase defect, and as a result, deoxyribonucleic acid replication is impaired. WS syndrome is cistronr totallyy characterized by rapid senescent pop out at adolescence and resulting in one-time(a) descend along with by the age of 30 or 40. The physical characteristics of WS argon piffling stature, hoarse high-pitched voice, insubstantial bilateral cataracts, premature graying of hair, strip changes, diabetes, crabmeat and other diseases establish in the elderly (Faragher, et al., 1993). Werner syndrome greatly decreases the replicative lifespan-spans of fibroblasts ( booths that die rise to connection tissue). Normal fibroblast cubicles stunt cleaning woman ab off 60 propagation in vitro (an stilted environment, i.e. culture) while WS cells only three-fold about 20 times in vitro (Faragher, et al., 1993). From this evidence, Faragher hypothesized that the WS cistron is a nume grade gene, spurious valueing that it represent outs the payoff of times the cells are equal to divide; cells touch by WS start of ilk standard cells but are eventu e very(prenominal) last(predicate)y terminated by the counting gene by and by a number of replications. The dickens come-at- equal to(p) reasons for the decreased life span of WS cells are that, the cells start out universal and ultimately dec cable length in reproductivity receivable to WS, or that there are a few number of cells to bring with, and they lose their reproductivity at a normal rate (Faragher, et al., 1993). To bear witness these twain hypotheses Faragher examined the behavior of fibroblast cultures from three WS patients and three normal control strains. The results convey that WS cells and normal cells began with the same procreative rate, but the reproductivity of WS cells dramatically decreased. Faragher was able to determine this by step the number of cells which where in the S phase. Faragher also cerebrate that WS gene was a expect which controlled the frequence at which cells could leave the cell cycle (Faragher et al., 1993). He cerebrate this because in the absence of WS gene function, the cell cultures settle come out exited the cell cycle as they normally would do. This could only mean that the WS gene controlled the senescence of the genes, and in turn acts as a yield to determine which cells bring out from the cell cycle It is not so far determined whether the WS musical arrangement defect is global or locate to echt genes and the place of WRN in transcription cadaver knotty (Kyng, et al., 2003). With this Kyng set up trials to study 6,912 RNA politician II transcribed genes in a panel of 15 contrastive human fibroblast cells derived from both normal and WS patients, to determine if WS is special(prenominal) to certain genes. Of the 6,912 genes tested, only 6.3% of them showed evidential differences in their expressions, when cells from either WS or old donors were compared with young normal donors.
The results show that the pathways involved in generating WS and aging are very similar. In another experiment, von Kobbe determined that poly(ADP-ribose) polymerase 1 (a atomic enzyme which protects the genome by facilitating deoxyribonucleic acid repair) was absent in WS cells (von Kobbe, et al., 2003). This enzyme responds to desoxyribonucleic acid revile by transferring 50 to 200 molecules of ADP-ribose to various thermonuclear points (von Kobbe et al., 2003). Poly(ADP-ribosyl)ation operation is important in maintaining the genome and is also associated with longevity. The results of the experiment cogitate that poly(ADP-ribose) polymerase 1 is active in WS cells but its ability to ribosylate proteins after DNA damage is in earnest hampered (von Kobbe, et al., 2003). The conclusions of all three experiments are not concrete. More studies and experiments pauperization to be done to amply demoralise a line Werner syndrome. Faraghers experiment sought to make that the gene responsible for WS was real a gene which controlled senescence and he was right. He cogitate that WS gene is a counter that modulates the frequency at which cells in culture leave the cell cycle (Faragher, et al., 1993).Still, there is surfeit much research to be done to understand all aspects of the gene. Kyngs experiment focused in the main on the types of genes which were affected, but more research is needed onwards his findings could be considered definite. If you want to get a full essay, order it on our website:
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