Doesn't successive DNA replication almost guarantee mutation?

Question

I don't know a thing about biology, but it seems to me that we all originate from a single fertilized egg cell that divides many times to become an adult organism. As I understand it, each time this division occurs, the nuclear DNA is replicated. Since there must be MANY such replications before we reach adulthood, and since each copy is a copy of a prior copy (with the exception of the original egg cell), it seems that the Law of Large Numbers would almost guarantee that errors would be introduced in future divisions. Since these errors are in turn propagated to future generations of cells within the organism, the number of errors would compound, and if the organism lived long enough (as measured in replication cycles), that it would have all sorts of things breaking down due to increasingly corrupted copies of its 'original' DNA. Does this actually happen in higher animals, or do the bad copies usually just die off since they aren't viable? Could this explain aging (in part)?

Answer 1

There are several good answers here. Don't forget that our cells also have DNA repair mechanisms.

Mutations definitely occur during each mitosis. Most are benign...
1. they code for equivalent amnio acids
2. they fall into a non-coding sequence
3. the abnormal protein coming from one or a even a whole line of cells makes no difference because there are many more cells around it making normal protein
4. the cell line with the mutation is in a tissue that does not require that particular code
5. when mutations are too many or too serious for DNA repair mechanisms to fix, some cell go to automatic cell death (apoptosis)

Cancer is occurs when mutations affect genes for DNA repair or those involved in signaling cells to replicate (or stop replication). Cancer cells have also "figured out" how to bypass apoptosis.

One theory about aging: during each mitosis, the ends of the DNA (telomeres) get shorter. Eventually they start to delete coding sequences.

Answer 2

Could. Mutation in the somatic cells do happen, but human somatic mutational rates are slow in comparison to other organisms. 10^-4 to 10^-6. Germ lines are a different story; for your progeny. Then there are mitochondrial rates that are much faster that the average eukaryote rate. Copies that are too "bad" would not be viable, but the mutations are epigenetic; either neutral or averaging out types. It is being looked at in the aging process, but it is to soon to make any firm pronouncements.

PS successive replication is a guaranty of random ( in no numerical order ) mutation. The rate, as I stated above is well understood and estimated. Copy errors happen to the best of us.

Answer 3

Great question, but I don't know if I can answer all of it in one sitting.

But first, keep in mind you have two templates of DNA from which your body works of off.

You have your own germ line DNA, which is to say your sperm DNA (assuming your a boy). It is haploid and was derived from meiosis, which in itself has its own rules for variations and mix-ups. This is what you will pass on to your children. Eventually it is the DNA template from which the rest of your cells will work off of for the rest of your life.

As an "egg" or zygote, your cells divide rapidly, but those germ line cells are separated from the rest of the cells and left to their own until you are ready to procreate.

The other cells, then, are called somatic cells. They divide rapidly, and give rise to your everyday body (flesh, muscle, bone).

But they acquire mutations, which are mainly governed by the environment and polymerase mistakes, and the such.

Just in theory only, when they acquire mutations in their DNA, they die.

Here is some more fun information, supplied to confuse things:

Somatic cells are said to arise from stem cells (SC). I don't think it is well established if the somatic SC's are lineage specific or not. But all somatic cells are suspected to acquire mutations like the rest of your cells.

Interestingly, one can locate SC's in a tissue specific organ, giving rise to the same lineage specific cells which are limited by telomerase (Hayflick's Limit) and hence succumb to apoptosis.

More interestingly, there seems to be evidence that SC's are capable of moving from one tissue specific organ to another. I am unsure of the antigens, or cluster designations (CD) these peculiar cells are expressing, but google searches can help you further.

So, theoretically, mutated SC's can give rise to mutated somatic cells. And they can move about within your body to give rise to different cell types.

To add to the complexity you have mitochondrial DNA (mtDNA) which has its own force on cell life (especially age related forces).

mtDNA also seems to be effected by mutations, but I suspect more environmentally, for somatic cells (since they are the one making you live day to day, and not the germ line cells).

In terms of germ line mtDNA, again, I'm not well schooled here.

But since inheritance of mtDNA seems to be a matter of cytokinesis, or a random and even division of cytoplasm, it seems the complexity is rather even between sexes.

But I think your question should be really focused on the proteins that manage the genetic material and it's replication (and there is quite a bit manage).

Scientist do suspect there are certain "gatekeeper" proteins that determine whether a cell will be allowed to replicate DNA or not.

If gatekeeper protein is saying "yes sir" all the time, then the cell can replicate "good DNA" and/or it can replicate "bad DNA".

If it is a "no sir" gatekeeper protein, then the cell cannot replicate any DNA.

This, naturally, is critical in a cell population expansion.

Points I may not have directly addressed in your question:

Their are two copies of each gene, one found on the pair of chromosomes, so if one goes bad there is a back up copy.

A bad copy gene beget of a good copy gene doesn't mean that suddenly the good copy goes away. The good copy is still there to be copied again in the correct way for about 60-70 times. One good copy that is made form the original will be dealt with the same way. Unfortunately, the bad copy might be copied 60-70 times too, diluting the effects of the good copy.

Original copies of genes come from both mom and dad, so if an offspring inherited one bad copy, the hope is that they would inherit one good copy from the other parent. This is the basis of genetic screening; Certain populations are known to be "high carriers of the dysfunctional gene", so breeding within that population may carry risk to the unborn child, in the sense that the child may not thrive.

One former theory about "corrupted" copy of genes is that SC's provide a new supply of uncorrupted cells. Most scientist now think that the SC's can obtain corrupt copies themselves, and ultimately be the source of bad DNA.

Google some more info using these key phrases to find out more (in random order):

Hayflick's Limit telomerase
gate keeper p53
Mitochondrial DNA Age
Apoptosis
Cell cycling

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Answer 4

Lot of mutations do occur although small percentage. But there are lot of repair mechanisms that actually correct mutations. In rare occasions mutation passed onto offspring is repaired after it is passed on.

And you know what cancer is right? Too many bad mutations and tumor growth can kill whatever animal.

Answer 5

You are on to something. Most of the errors do just die. Then we have cancer. Then we have organ failure. There are things in place to control errors. They too are not infallible. Many changes/errors are harmless and unnoticed. Have you noticed subtle differences in twins?

Answer 6

there are also many many many different repair mechanisms the cell has to check and recheck itself.