Replicative cell senescence

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Replicative cell senescence is a process that involves the shortening of [[Telomere|telomeres]] (regions at the end of chromosomes). This occurs as in most somatic cells [[Telomerase|Telomerase]] (an enzyme that prevents the telomeres shortening by solving the end replication problem) is turned off. This means that in each replication a small region of the telomere is lost each time as the ends cant be replicated without the presence of Telomerase. This mechanism is used to prevent cancers by ensuring cells have a finite lifespan.&nbsp;The senescent state is generally reached after 50 cell divisions, with the cells being able to sustain themselves, however not to replicate any further. It has been widely proposed that replicative cell senescence may be linked to ageing; evidence suggests a close relationship between average telomere length and an individual’s age, with certain premature ageing diseases (such as Progeria) being associated with relatively shortened telomeres. Despite the preventative effect of replicative senescence against tumours, in the case of many cancers telomerase is reactivated, therefore granting the malicious, uncontrollably-dividing cells biological immortality. An experimental verification of this theory was the fact that once grown in vitro with a supply of active telomerase, mammalian fibroblasts (connective tissue cells) grown had a significant delay in senescence.<ref>Brown T., (2012) Introduction to Genetics: a Molecular Approach, (I. Title) New York: Garland Science (p.224-225)</ref><br>  
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Replicative cell senescence is a process that involves the shortening of [[Telomere|telomeres]] (regions at the end of chromosomes). This occurs as in most [[Somatic_cells|somatic cells]] [[Telomerase|Telomerase]] (an enzyme that prevents the telomeres shortening by solving the end replication problem) is turned off. This means that in each replication a small region of the telomere is lost each time as the ends cant be replicated without the presence of Telomerase. This mechanism is used to prevent cancers by ensuring cells have a finite lifespan.&nbsp;The senescent state is generally reached after 50 cell divisions, with the cells being able to sustain themselves, however not to replicate any further. It has been widely proposed that replicative cell senescence may be linked to ageing; evidence suggests a close relationship between average telomere length and an individual’s age, with certain premature ageing diseases (such as Progeria) being associated with relatively shortened telomeres. Despite the preventative effect of replicative senescence against tumours, in the case of many cancers telomerase is reactivated, therefore granting the malicious, uncontrollably-dividing cells biological immortality. An experimental verification of this theory was the fact that once grown in vitro with a supply of active telomerase, mammalian fibroblasts (connective tissue cells) grown had a significant delay in senescence.<ref>Brown T., (2012) Introduction to Genetics: a Molecular Approach, (I. Title) New York: Garland Science (p.224-225)</ref><br>
  
 
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Revision as of 14:07, 20 October 2016

Replicative cell senescence is a process that involves the shortening of telomeres (regions at the end of chromosomes). This occurs as in most somatic cells Telomerase (an enzyme that prevents the telomeres shortening by solving the end replication problem) is turned off. This means that in each replication a small region of the telomere is lost each time as the ends cant be replicated without the presence of Telomerase. This mechanism is used to prevent cancers by ensuring cells have a finite lifespan. The senescent state is generally reached after 50 cell divisions, with the cells being able to sustain themselves, however not to replicate any further. It has been widely proposed that replicative cell senescence may be linked to ageing; evidence suggests a close relationship between average telomere length and an individual’s age, with certain premature ageing diseases (such as Progeria) being associated with relatively shortened telomeres. Despite the preventative effect of replicative senescence against tumours, in the case of many cancers telomerase is reactivated, therefore granting the malicious, uncontrollably-dividing cells biological immortality. An experimental verification of this theory was the fact that once grown in vitro with a supply of active telomerase, mammalian fibroblasts (connective tissue cells) grown had a significant delay in senescence.[1]

References

  1. Brown T., (2012) Introduction to Genetics: a Molecular Approach, (I. Title) New York: Garland Science (p.224-225)
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