Guardian: Telomere Timebomb: A Potential Explanation for Species Extinction?

[FZ+]

Has anyone read this?

http://www.guardian.co.uk/life/feature/story/0,13026,1187579,00.html

Stindl argues that the protective caps on the end of chromosomes, called telomeres, provide the answer. Like plastic tips on the end of shoelaces, all eukaryotic species have telomeres on the end of their chromosomes to prevent instability. However, cells seem to struggle to copy telomeres properly when they divide, and very gradually the telomeres become shorter. Stindl's idea is that there is also a tiny loss of telomere length between each generation, mirroring the individual ageing process.

Once a telomere becomes critically short it causes diseases related to chromosomal instability, or limited tissue regeneration, such as cancer and immunodeficiency. "The shortening of telomeres between generations means that eventually the telomeres become critically short for a particular species, causing outbreaks of disease and finally a population crash," says Stindl. "It could explain the disappearance of a seemingly successful species, like Neanderthal man, with no need for external factors such as climate change."

To my eyes, this is a potentially huge development. Does anyone know more about this? How credible is his claims?

 

[chroot]

This is exceptionally old news. Telomeres have been known and understood for a very, very long time. They are but one of the many mechanisms by which cells age.

- Warren

 

[hitssquad]

No one has ever proposed before that telomeres shorten between generations within a species.

 

[chroot]

Ah, I didn't read the quote very thorougly. AFAIK, telomeres do not get shortened in meiosis, so gametes aren't affected. Or so I thought.

- Warren

 

[Ivan Seeking]

Is Telomere Erosion a Mechanism of Species Extinction?
REINHARD STINDL
Institut fu¨r Medizinische Biologie, Medizinische Universita¨t Wien Wa¨hringerstrabe
10, 1090 Vienna, Austria.

PDF:
http://www.meduniwien.ac.at/user/telomer/pdfs/Stindl_PP_2004b.pdf

HTML:
http://www.google.com/search?q=cache:YhWwkVwGf-kJ:www.meduniwien.ac.at/user/telomer/pdfs/Stindl_PP_2004b.pdf+telomere+%22chromosomal+instability%22+Stindl&hl=en&ie=UTF-8

 

[Monique]

The question would be whether gamete cells have any telomerase activity.

I think they do. I once wrote an assay a long time ago, and the only time that telomeres don't shorten is during embryonic development. The enzyme telomerase is expressed that stops the shortening of the telomeres by adding pieces of telomere to the tip of the chromosomes.

Now they have to find out how efficient that process is and whether there still is residual telomerase activity in the germ cells of an organism.

Cancerous cells also express the enzyme telomerase and thereby become immortal.

 

[Tsu]

Cancerous cells also express the enzyme telomerase and thereby become immortal.

Do you know of anyone using this fact to research the possibility of using this enzyme to fight cancer? It just strikes me as a distinct possibility... You know - block the enzyme and the cell can't do it's thing and eventually dies?...

 

[Monique]

When I wrote the assay there definitely were papers looking into this. Since the telomeres of cancer cells ARE much shorter than other body cells, so they would be the ones to die first since they divide so fast. But there are other cells in the body that naturally have telomerase activity.. if I remember correctly, those were the germ cells and the stem cells for sure.

I should find that assay again.. it is somewhere in a large pile of papers in some cardboard box.. or somewhere on another continent.. ohwell.

I'd have to check some of the recent literature if they made any significant progress.

 

[toloXXX]

Only to add, :-)

First, if you like, you should check out "Nonhuman Primate Models in Biogerontology" by mark A.lane or "How to defy death" by Nell Boyce to get some more information...

These days, my friend is going on "business" :), I have a chance to use his books and many other things even his computer, :p


I think, tolomerase is not a strong antigen, in order to make an effective, broadly applicable cancer vacine, we will need to optimize and possibly combine it with other antigens. British and Swiss reseachers found a genetic switch that allows cancerous cells to flip the tolomerase switch back on after they have been odered by anticancer genes to flip it off. Blocking this process cuts off the enzyme and causes cancerous cells to stop multiplying. They also reported that they believed sooner or later, a drug can be found that targets the gene and keeps the tolomerase production switched off...


L'absence est à l'amour ce qu'est au feu le vent;
Il éteint le petit, il allume le grand.