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In my biology book I read about an experiment where the genes encoding telomerase were 'knocked out', but they could still live a normal life and no adverse effects were noticed until the 6th generation of offspring (although it did not say what the effects were).

I have often often heard how longer telomeres indicate longer life potential, but what happens when you run out of them? Would rapidly proliferating cells be affected before others? Do the cells then just stop dividing or would they continue to divide? If they continue to divide what would the effects be?

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do you have a link to the study that 'knocks out' the telomeres and finds the cells to not have any adverse affects? As I understood it the cells either enter a state of permanent cell-cycle arrest (senescence) or apoptose (programmed cell death) when they reach their Hayflick limit (i.e. when their telomeres run out). –  Luke Jun 18 '12 at 18:10
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A figure in the book taken from 6th generation telomerase deficient mice was taken from: Cell, Blasco, M. A., ‘Telomere shortening and tumor formation by mouse cells lacking telomerase RNA’, 91, pp. 25–34 –  Ultimate Gobblement Jun 18 '12 at 18:38
    
I'm a student of Alevels n while preparing for my biology mcqs related to the chapter of cell division, came across an mcq.. "Chromosome telomeres promote DNA replication and are not completely replaced during mitosis. A substance X is known that completely replaces telomeres during mitosis. What will be the effect of growing a cell culture with and without substance X? Rhe answer was:The cells didvide continuosly with substance X and cell division eventually slows and stops without substance X. But I don't really understand the answer..why is this the answer? Please help me out if you underst –  user4465 Sep 14 '13 at 7:13
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@Taleah Please don't "hijack" questions to ask your own question, especially not if they are a year old. Your can ask this as an own question, tag it with "homework" and specify what you tried to answer the question. –  skymninge Sep 16 '13 at 13:03

1 Answer 1

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

  • This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.

  • So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.

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