mutatin bonding

[ann]

I have just read that gene mutations can be additions ,deletions or subsitutations of the base sequence. If this occurs during DNA replication How do these new bases form hydrogen bonds with the existing original strand if A only bonds with T and G only bonds with C ? Thanks

[CharonY]

They usually don't. Mutations normally manifest themselves after a replication step.

 

Example imagine the following pairing:

 

ACGT

||||

TGCA

 

Now one point mutation occurs:

 

ACGG

|||

TGCA

 

The G-A do not form hydrogen bonds, but after replication both daughter strands will show differences:

 

ACGG

||||

TGCC

 

and the unmutated strand will be like the original again:

ACGT

||||

TGCA

[vampares]

I think *most* mutations are Repeat Expansions. "Fragile X" explanations may help.

 

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There is a state of heterochromatin that utilizes repeats: For example, all human chromosomes 1, 9, 16, and the Y chromosome contain large regions of constitutive heterochromatin. This is as opposed to Euchromatin which does not use these repeats. In cells there is a "change" or Epigenetic Inheritance overtime. I don't know what role this plays exactly but you can follow along to see how changes can occur -- some good, perfectly normal, natural aging process -- others bad for the cell but otherwise nothing comes of them like cancer or anything. Involved in this could be Satellite DNA, Paramutation, Gene silencing, Transvection and my personal favorite Nonsense Mediated Decay.

 

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Anyways these Trinucleotide repeat expansions (whatever their origins) are often looped when the DNA helix's. Why, how they got their -- I don't know -- but they (something) seems to have effected the protein that is assigned the good job of regulating the DNA. I think it is the BRCA1 aka polyQ or poly glutamine. If you browse this locus alternating morbidity/pheno/gene_seq sorting, scroll up and down -- you'll see "huntingtin type 1" (or Huntinton's is sameting), some structural genes etc. all clustered there on the same block of squidgable DNA. Also there is also a chromosome 17 frame index -- may be involved with heterochromatin like functionality.

 

But most of goofy sh*t has already been processed into the DNA when you get it. I don't know how all of this happens after expansion -- the DNA may be "repaired" by the system to make it fit into a helix. At which point adding (that is repeating this new mistake to make it even) or deleting is done..

 

They say "what you don't know, can't hurt you." It may be true. Few mutations will give you cancer. They also say everyone is of good humor and rather jovial, free spirits -- this is with no teeth, weird hair, slightly retarded and having to hold your eyelids up with something. And watch what you eats too!

 

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This TATA box binding protein has been linked to degenerate sequencing. Note the BRCA1 gene.

 

 

This is a mutation frequency graph from the linked article about Homologous Recombination (HR), and the contrasting Non-Allelic Homologous Recombination (NAHR). Impotence is a possible result.

 

Anyways SNP is a relatively rare event, bordering on extremely rare. The number of generation that would need to be genetically analyzed in a cloned cell line -- much less one that undergoes genetic recombination -- would be prohibitive in the laboratory environment. It could just as plausibly be space aliens as any given mechanism in a proper organism.