End-replication problem help?

Question

End-replication problem help?

Answer 1

Look up 'telomerase' in wikipedia for some more info but i can tell you yes telomeres shorten with each division, yes telomerase adds bits on to solve the problem. In adults, cells which undergo alot of division have greater quantities of telomerase to keep them viable. in cells which undergo less or no division then telomerase levels are very low. Getting old is more complicated than just the telomere problem, though telomerase has been implicated in premature-aging dieseases. I'm sure there are plenty of contributing factors other than this, but I would say that as you get older your cells will accumulate mutations making them inviable or could give you cancer. Experiments in mice with telomerase to see if they could slow the ageing of the mice showed that the mice got cancer more frequently so did not prolong their lives.

Answer 2

I've put a link to a great site below.

Answer 3

errrr. try....



work hard

Answer 4

try biology.com, wikipedia.org, or type the questions on a search engine!

Answer 5

1. Have a look at at this abstract:



Mol Cell Biol. 2001 Sep;21(17):5753-66.

In vitro reconstitution of the end replication problem.

Ohki R, Tsurimoto T, Ishikawa F.



The end replication problem hypothesis proposes that the ends of linear DNA cannot be replicated completely during lagging strand DNA synthesis. Although the idea has been widely accepted for explaining telomere attrition during cell proliferation, it has never been directly demonstrated. In order to take a biochemical approach to understand how linear DNA ends are replicated, we have established a novel in vitro linear simian virus 40 DNA replication system. In this system, terminally biotin-labeled linear DNAs are conjugated to avidin-coated beads and subjected to replication reactions. Linear DNA was efficiently replicated under optimized conditions, and replication products that had replicated using the original DNA templates were specifically analyzed by purifying bead-bound replication products. By exploiting this system, we showed that while the leading strand is completely synthesized to the end, lagging strand synthesis is gradually halted in the terminal approximately 500-bp region, leaving 3' overhangs. This result is consistent with observations in telomerase-negative mammalian cells and formally demonstrates the end replication problem. This study provides a basis for studying the details of telomere replication.



Let me know if you want the paper (email me)



2.Telomerase is an enzyme that adds telomere repeat sequences to the 3' end of DNA strands. By lengthening this strand DNA polymerase is able to complete the synthesis of the "incomplete ends" of the opposite strand. It is a is a ribonucleoprotein and a reverse transcriptase; synthesizing DNA from an RNA template.



Fully differentiated cells do not prduce telomerase.



Telomerase is generally found only in



the cells of the germline, including embryonic stem (ES) cells;

unicellular eukaryotes like Tetrahymena thermophila;

some — perhaps all — "adult" stem cells and "progenitor" cells enabling them to proliferate;

cancer cells.



When normal somatic cells are transformed in the laboratory with DNA expressing high levels of telomerase, they continue to divide by mitosis long after replicative senescence should have set in. And they do so without any further shortening of their telomeres.



The lack of telomerase in adult cells lead to the natural shortening of the telomeres, and, consequently, to cellular senescence and ageing.



This is a beutiful review on the topic http://hmg.oxfordjournals.org/cgi/content/full/10/7/677

which should also answer your 3.rd question