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Im no expert or anything but Im wondering if theres any chance epigenetic factors, such as histones or chromatin, could force the dna to be overall excessive or inexcessive, thereby forcing the dna to be reduced or expanded upon.

Like what happens if theres too much histones trying to coil the dna, to the point where the dna cannot be tighter and it would break, would it then be repaired and elongated or would it abandon some histones to prevent a break?

Or if not enough chromatin for the dna, if the dna reduces its size.

If possible I'd like to know in reference of reproduction.

Also if theres too few histones, I figure itd just mean the dna is being expressed more.

But if histones and chromatin are monitored by dna anyways then epigenetic influences are actually indirect genetic influences, so I am assuming thats not the case. But it could be.

Enlighten me? With links if possible, so I can understand it with visuals I suppose.
Mutations mainly occur during DNA replication so you've got to split the strands and make copies and that anyway. By my understanding that rules it out.

It wouldn't really be useful though, as utilizing it would have to be a response and by the time you want mutants natural selection is already bearing down on you.

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Transcriptionally active euchromatic regions are more prone to transcription-associated mutations, which are mutations that occur when the DNA is been transcribed.


Transcriptionally inactive heterochromatic regions become heavily methylated. Deamination of cytosine is a common reaction in which the amino group is replaced by a carbonyl group in cytosine. In a normal cytosine, deamination produces uracil which can be recognized by the repair system. However, a methylated cytosine that undergoes deamination will turn into thymine, which cannot be repaired as easily.


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I am unaware of any studies looking specifically at the effect of nucleosome wrapping dynamics on mutation. But I would not be surprised if from time to time a double stranded break occurs from a nucleosome wrapping to tightly.

Chromatin structure does play an important role in mutation. For example, the parasite that causes malaria is very prone to mutations due to double strand break. A study looked at the locations of these breakages and found that they occurred primarily in the linker regions (the strings of DNA linking the nucleosomes).

Malaria parasite: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC310281/pdf/nar00039-0245.pdf
In terms of epigenetics, DNA breakage is due to over condensation of histones is highly unlikely to be heritable. Such breakage would have to have been expressed in the maternal cell which would be highly deleterious.

However, if you are asking about DNA repair mechanisms causing mutation, then yes, that occurs often. It is easily seen in skin cancer where the DNA is damaged by UV rays, which causes breakage in the DNA sequence. DNA repair mechanisms may improperly match DNA sequences together which causes genes involved in replication to be mutated.

If there wasn't enough histones in a cell then, more DNA sequence would be available for transcription. However, it is doubtful if that would occur in a real system since roughly half of a cell's histones are inherited from the maternal cell. As well as, the cell wouldn't be able to manage its energy consumption if most of its genes are activated or able to be activated at the same time.

Chromatin remodeling and histone modification are regulated by genetics. What makes epigenetics interesting is that the histone modifications that occur during a maternal cell life is heritable.

As for references, looking in any molecular biology textbook under histone modification/chromatin remodeling should be able to help you out. A book that I personally use on the subject is Molecular Biology of the Gene by Watson, etc. It has plenty of visuals to go along with tons of information.

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