DNA Question... 2 questions.

[RyanJ]

Hi there everyone!

 

I have two questions.

 

After talking to my biology teacher about something not even related to this we some how ended up on the topic of ageing and how the "sticky" ends of the chromosomes are not correctly coppied. If [acr=Deoxyribonucleic acid]DNA[/acr] is supposed to be error checked while the base pairs are being matched up then why are these ends not always correctly copped as most of the other [acr=Deoxyribonucleic acid]DNA[/acr] is? Is it because humans are designed to age in this way or is it a flaw in the way the [acr=Deoxyribonucleic acid]DNA[/acr] replicates?

 

Also, how do cells know when to start meitosis, do they have some sort of inbuilt timer or are they driven by horemones or a combination of the two?

 

Thanks for the help,

 

Ryan Jones

[Dak]

test

 

buggerit... why wont it let me post my response?

 

hang on, ill try to edit it in in installments. [edit]done[/edit]

 

Question 1:

 

due to the way that DNA polymerase works, it is not possible for it to copy a strand of DNA all the way to the end, resulting in the copied strand being slightly shorter than the original.

 

This is because the foremost part of DNApolyIII is used as an engine, to pull the rest of the enzyme -- including the bit that does the copying, located to the rear -- along the existing DNA strand like a train along tracks. At the 3' end of the strand of DNA, DNApolyIII 'runs out of track', and cannot copy any further.

 

[b]Figure 1 -- DNApolyIII at the end of the line[/b]

KEY: 
=                            --  DNA
[color=red]left part of DNA polymerase[/color]  -- Bit that does the copying
[color=blue]right part of DNA polymerase[/color] -- bit that pulls the DNApoly along

          ___________________
          [color=red]|---------|[/color][color=blue]|-------|[/color] [b]}--DNA polymerase, moving thataway -->[/b]
===============================
=====================

At the point shown above, DNA polymerase has run out of DNA to pull itself 
along on, and so cannot move (and thus copy) further upstream.

 

To circumvent this, chromosomes end in a telomere -- a non-coding stretch of repetative DNA (CCCTAAA in the case of humans).

 

So, when the dna is copied, the telomere will be a bit shorter in the new strand than in the original. this is reversed by telomerase, which whacks in a few more CCCTAAA repeats to bring the telomere back up to the correct size.

 

like this:

 

[b]Figure 2 -- telomerase doin' its thang[/b]

[color=red]|[/color]                                         [color=red]|[/color]
[color=red]|[/color]                      [color=red]|[/color]                  [color=red]|[/color]
[color=blue]|[/color]---->DNA polymerase-->[color=blue]|[/color]---->telomerase-->[color=blue]|[/color]
[color=blue]|[/color]                      [color=blue]|[/color]                  [color=blue]|[/color]
[color=blue]|[/color]                      [color=blue]|[/color]                  [color=blue]|  [/color]

[color=blue]coding DNA[/color]  
[color=red]Telomeric, non-coding DNA[/color]

 

 

The reason that telomerase can do this is that it doesnt have to move along, or even copy, the DNA from the origial strand as it knows the DNA will be CCCTAAA (or GGGATTT), which the enzyme reverse-transcribes from an RNA template located inside the enzyme intself, thus circumventing the 'cant copy at the end of the chromosome' problem.

 

Anyway, if something goes wrong with this, the telomeres will become shorter and shorter with each replication, untill eventially a little bit of coding DNA is lost from the end of the chromosome every time that the DNA is replicated.

 

The reason that proof-reading doesnt catch these errors is that the proof-reading is done at more-or-less the same time as the DNA copying, the proof-reading enzymes following the replicative enzymes along as they copy the DNA (is the simplified version).

 

as the 3' end isnt copied by the normal enzymes in the normal way, the proof-reading isnt carried out on it.

 

Anyway, one strand of the telomer is supposed to be longer than the other and form a double strand with itself... thus making error-checking it for length pretty dificult.

 

Cells seem to cope with this by relying on the fact that telomerase may elongate the shortened telomer either too much or too little, and overall the length of the telomere remains dynamically steady, ie it will randomly increase and decrease in size, but remain roughly the same length over time.

 

this obviously doesnt work brilliantly, as old people quite oftern are lacking telomeres

 

Question 2:

 

Chemicals.

[RyanJ]

Great Description Dak, it helped a lot! If they even find an enzyme that could act like DNA plymerase but could copy all the way to the end of the chromosome then what difference would that have?

 

 

Chemicals.

 

So' date=' are they caused by something like a hormone or, by a "chemical clock" inside the cell? Both can still apply but I'm guessing that it varies in different curcumstances.

 

And congradulations on yout 1,200[sup']th[/sup] post!

 

Cheers,

 

Ryan Jones

[Dak]

Great Description Dak, it helped a lot! If they even find an enzyme that could act like DNA plymerase but could copy all the way to the end of the chromosome then what difference would that have?

 

Hmm... im not sure that would allow telomeres to be done away with. as well as solving the shrinking chromosome problem, they have a few other roles... most notably, they protect the ends of chromosomes from damage (the long strand of the telomere folds up into a knot, and anyway the telomere can bear a little damage as its non-coding). without telomeres, the chromosomes would likely shrink anyway due to wear and tear.

 

So, are they caused by something like a hormone or, by a "chemical clock" inside the cell? Both can still apply but I'm guessing that it varies in different curcumstances.

 

there was a reason that my answre was only one word long: I switched off during my lectures on the regulation of the cell-cycle due to an incredibly booring lecturer... i just remember it being something complicated involving lots of chemical checkpoints.

 

And congradulations on yout 1,200^th post!

 

Cheers, but my posts in the 'test' thread got deleted by mokele, so im back down to <1,200 again now

[RyanJ]

there was a reason that my answre was only one word long: I switched off during my lectures on the regulation of the cell-cycle due to an incredibly booring lecturer... i just remember it being something complicated involving lots of chemical checkpoints.

 

Ah, right I see. I'm guessing it does involve both a chemical timer and a hormone - it makes sence. In mitosis anyway because hormones are released during the teen years that make the body grow and change a lot. And then again when you are younger the same hormones are not present but the cells still replicate pointing to the conclusin they have a clock mechanism

 

Cheers & get your 1,200 posts back

 

Ryan Jones

[donkey]

Proteins called cyclins are involved with cell cycle timing. It'd be easiest just to quote wikipedia:

 

Cyclin is a protein involved in the progression of cells through the cell cycle. It forms a complex with the cyclin-dependent kinase (Cdk), which activates the latter's protein kinase function. Cyclins are so named because their concentration varies in a cyclical fashion during the cell cycle; they are produced or degraded as needed in order to drive the cell through the different stages of the cell cycle

 

http://en.wikipedia.org/wiki/Cyclin

[RyanJ]

Thanks for the link donkey, I'll aheva read when I finish my Chemistry homework

 

Cheers,

 

Ryan Jones

[treva]

Proteins called cyclins are involved with cell cycle timing. It'd be easiest just to quote wikipedia:

 

 

 

http://en.wikipedia.org/wiki/Cyclin

 

But it all starts with a growth factor binding a cellular receptor. This initates a cascade that eventually leads to the synthesis of proteins involved in DNA replication and mitosis.