Serviços Personalizados
Journal
Artigo
Indicadores
Citado por SciELO
Links relacionados
Similares em SciELO
Compartilhar
Medicina (Buenos Aires)
versão impressa ISSN 0025-7680versão On-line ISSN 1669-9106
Resumo
ROSETE, María; PADROS, María Rosa e VINDROLA, Osvaldo. The nucleolus as a regulator of cellular senescence. Medicina (B. Aires) [online]. 2007, vol.67, n.2, pp.183-194. ISSN 0025-7680.
The nucleolus has been considered originally only as the site for the ribosome synthesis, but now it is well known that it represents a dynamic nuclear structure involved in important cellular processes. Several evidences have demonstrated that the nucleolus regulates the cellular senescence. Specific mutations on the DNAs codifying for nucleolar proteins induced premature senescence from yeast to human. The failure to repress the genes transcription codifying for damaged rRNA, and the mutations in DNA helicases, which minimizes the formation of DNA extra-chromosomal circles codifying for rRNA, modify the nucleolar structure and induce premature senescence in yeast. Similarly, in humans, the reduction of these DNA helicases levels, which are localized in the nucleoli and participate in maintenance of genomic integrity, helps to the development of those diseases associated with premature senescence. Furthermore, the presence in the nucleolus of some telomerase components, indicates that part of the biosynthesis of this enzyme occurred in this nuclear structure; suggesting a communication between the nucleolus and the synthesis of the telomeres in the regulation of cell senescence. On the other hand, the nucleolus sequesters proteins to regulate its own biological activity, from the start to the end of cellular replication. In addition this nuclear structure is involved in the biosynthesis of most cellular ribonucleoprotein particles, as well as in cell cycle regulation, making it central to gene expression. In conclusion, the nucleolus became a multifunctional subnuclear structure involved from cell proliferation to cell senescence.
Palavras-chave : Nucleolus; Aging; Werner syndrome; P53; Telomeres.