The "seesaw" effect of spontaneous methyl cytosine deamination and gBGC causes epigenetic adaptation without Darwin


The seesaw effect of spontaneous methyl deamination and gBGC (bGC) conversion is a phenomenon that occurs in DNA methylation for the non Darwinian epigenetic control and adaptation of the organism.

Both these processes are teleological in that they are not random as with NeoDarwinism rather they are "built in" cellular mechanisms.

These two teleological processes can counteract each other, resulting in a stable level of methylation for epigenetic adaptation.

Spontaneous methyl deamination is the process by which a methyl group is removed from a cytosine residue in DNA. They account for 40% of all mutations and are the most common nucleotide mutation. They occur as a "biased" non random nonDarwunian mutation.

This can happen spontaneously, or it can be induced by environmental factors such as exposure to chemicals or radiation. bGC conversion is the process by which a cytosine residue is converted to a guanine residue.

When spontaneous methyl deamination occurs, it results in the loss of a methyl group from a cytosine residue. This can lead to a decrease in the level of methylation at that site. 

However, bGC conversion can counteract this effect by converting the cytosine residue to a guanine residue, which is not methylated.

As a result of this seesaw effect, the overall level of methylation in DNA can remain stable, even in the face of changes in the rate of spontaneous methyl deamination or bGC conversion. 

This is important for maintaining the epigenetic regulation of genes, as changes in methylation can have a significant impact on gene expression.

The seesaw effect of spontaneous methyl deamination and bGC conversion is involved in gene regulation and is affected by environmental factors outside of Darwin's natural selection.

gBGC works by first identifying the uracil that has been produced by cytosine deamination. 

This is done by the enzyme uracil-DNA glycosylase (UDG). UDG removes the uracil from DNA, leaving a single-stranded gap. This gap is then filled in by DNA polymerase, which uses the complementary strand of DNA as a template.


gBGC is a very efficient DNA repair pathway, and it is able to repair cytosine deamination damage with a high degree of accuracy.

Overall, gBGC is a very important DNA repair pathway that helps to protect cells from the harmful effects of cytosine deamination.

gBGC can help to spread "biased"point mutations that result from cytosine deamination. 

Cytosine is a genetic "wild card." it's as if it has it's own code outside of DNA.


gBGC can help to spread these point mutations by copying the mutated DNA sequence from one cell to another. This can happen when two cells are physically linked together, such as in a cell culture. Or, it can happen when two cells are genetically identical, such as in a clone.

These "biased" teleological mutations can lead to NonDarwinian epigenetic adaptation.

The interplay of spontaneous deamination of cytosine and gBGC (bGC) bias can cause rapid epigenetic  adaptation.

First, deamination of cytosine can lead to the formation of uracil, which can then be misrepaired as thymine. This can result in a G-T transversion mutation, which can change the amino acid sequence of a protein. This teleological guided mutation can cause adaptation.

Second, bGC bias can affect the rate of deamination of cytosine. In general, cytosines that are followed by guanines are more likely to be deaminated than cytosines that are followed by other nucleotides. This is because bGC bias creates apurinic/apyrimidinic (AP) sites, which are more susceptible to deamination. AP sites are created when a DNA base is lost, and they can be repaired by a variety of mechanisms. However, some of these repair mechanisms can introduce mutations, which can also lead to adaptation.

Third, the interplay of deamination and bGC bias can affect the epigenetic  expression of genes. For example, if a cytosine is deaminated in a promoter region, it can change the binding affinity of transcription factors, which can then affect the transcription of the gene. This can lead to changes in the non Darwinian epigenetic expression of the gene for adaptation of the organism.

Overall, the interplay of spontaneous deamination of cytosine and bGC bias can be a powerful force for adaptation. By changing the DNA sequence or the expression of genes, these processes can allow organisms to adapt to new environments or challenges.

Here are some examples of how the interplay of spontaneous deamination of cytosine and bGC bias can cause adaptation:

  • In bacteria, deamination of cytosines in the promoter regions of genes can lead to changes in the expression of those genes. This can allow bacteria to adapt to different environmental conditions, such as changes in temperature or nutrient availability.

  • In humans, deamination of cytosines in the DNA of the immune system can lead to the production of new antibodies. This allows the immune system to adapt to new pathogens.

  • In plants, deamination of cytosines in the DNA of chloroplasts can lead to changes in the expression of genes involved in photosynthesis. This allows plants to adapt to different light conditions.

The interplay of spontaneous deamination of cytosine and GC-biased gene conversion (gBGC) is thought to have played a significant role in the early adaptation of life on Earth.

This is because cytosine deamination is a relatively common event, and it can lead to the accumulation of mutations in DNA. gBGC can help to fix these mutations, which can help to maintain the genetic stability of the organism.

In addition, gBGC can also help to create new genetic diversity. This is because it can spread biased point mutations to other parts of the genome. This new genetic diversity can then be used for new traits for adaptation.

As a result of these two factors, the interplay of cytosine deamination and gBGC is thought to have played a significant role in the early adaptation of life on Earth. This interplay continues to play a role in the NonDarwinian epigenetic adaptation of life today.

Articles

Spontaneous deamination

https://www.diigo.com/user/vmancha?query=%22spontaneous+deamination%22

bGC

https://www.diigo.com/user/vmancha?query=bGC

https://www.diigo.com/user/vmancha?query=gBGC


gBGC: A Mechanism for Spreading Point Mutations: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3208776/

Cytosine Deamination and gBGC in Cancer: https://www.nature.com/articles/nrc2731

gBGC: A Review: https://www.frontiersin.org/articles/10.3389/fgene.2018.00036/full

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