Senescence.doc

2 Pages
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Department
Anatomy and Cell Biology
Course Code
Anatomy and Cell Biology 4411B
Professor
Gannareddy

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Description
Senescence • Cells cannot proliferate indefinitely - they do not divide despite nutrients, growth factors and space • These cells are neither mitotic or post-mitotic cell and are different from prolifer- ative and differentiated cells •Altered morphology in culture •Growth-arrest (typically in G0 due to high levels of cell-cycle inhibitors) •Resistance to apoptosis (resistant to loss of growth factors, susceptible to FasL) •Altered gene expression (increase the expression of p16 and p21, de- creased expression of c-fos and cyclins) •Causes of cellular senescence • Telomere-dependent senescence - stretches of repetitive DNA and associated proteins that cap the ends of linear chromosomes and protect them from degradation or fusion by DNA-repair processes. Cell lose 50-200 base pairs of telomeric DNA during each S-phase. The end-replication problem will eventu- ally render the telomeres too short and critically non-functional. This causes cells to not proliferation indefinitely because the lack of telomeres will cause DNA damage and the cell will senesce. • DNA damage will also cause senescence. This depends on p53, p16 and p21. • Senescence caused by chromatin perturbation - chromatin state determines the extent to which genes are active (euchromatin) or silent (heterochro- matin). Histone deacetylase inhibition (HDAi) is thought to induce senes- cence. One possibility is through the upregulation of p21 and p16. • Oncogene-induced senescence - normal cells respond to many oncogenes by undergoing senescence. • Stress and other inducers of senescence - oxidative damage and inappropri- ate extracellular conditions cause senescence •Senescence growth arrest is established and maintained by p53 and p16-pRb tu- mour suppressor pathways. •p53 is constantly synthesized and is usually titrated away by Mdm2 w
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