Epigenetics challenges Junk DNAs Common Ancestry

There was never a time when genetics lacked epigenetics. Epigenetics acts as the megaphone of the environment over the gene.



"Transposons (TEs) are among the least investigated components of genomes."


The theory of Junk DNA considered TEs as "useless" discouraging further study. 


Non-autonomous transposable elements (TEs) are DNA sequences that can move from one location in the genome to another, but cannot do so on their own. They rely on the machinery of autonomous TEs and epigenetics to be mobilized. Non-autonomous TEs are much more common than autonomous TEs, and they make up the majority of TEs in most genomes.

Before epigenetics, it was thought that non-autonomous transposable elements (TEs) were mobilized by other active autonomous TEs only. This is because non-autonomous TEs lack the genes necessary for transposition, so they were thought to rely on the proteins produced by autonomous TEs to move.

However, with the discovery of epigenetics, it became clear that there are other factors that can influence the mobility of non-autonomous TEs.

As a result, we now know that the mobility of non-autonomous TEs is a complex phenomenon that is influenced by both genetic and epigenetic factors.


Here are some examples of how epigenetics can influence the mobility of non-autonomous TEs:

  • DNA methylation can silence the expression of autonomous TEs, which can prevent them from producing the proteins that are necessary for the transposition of non-autonomous TEs.

  • Histone modifications can make non-autonomous TEs more or less accessible to the proteins that are necessary for transposition.

  • The epigenetic state of the genome can also influence the rate at which new TE insertions occur. 


Overall, the discovery of epigenetics has revolutionized our understanding of TE mobility. We now know that TEs are not simply "Junk DNA " controlled by their own genetic code. Instead, their activity is complexly regulated by both genetic and epigenetic factors.

For year's Non-autonomous transposable elements (TEs) were used to suggest common ancestry before the discovery of "functional" Junk DNA and epigenetics. This was when they were thought to be "immobile" Junk DNA. As such they were thought  to be genetic "fossils" stuck in the Junk DNA. 

Now we know that 98% of TEs are within 1,000 base pairs of active genes. This is because TEs control those neighboring genes. 

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They are far from being Junk DNA as such they are not genetic fossils.

This immovable fossil idea is no longer true now we know it's not only autonomous TEs alone that guide non-autonomous TE insertions rather epigenetics as well.

When a non-autonomous TE inserts into a new location, it carries with it a sequence of DNA from its previous location. This sequence of DNA is called a target site duplication (TSD). 


Over time, TEs can accumulate mutations, but the TSDs remain relatively unchanged, likely due to epigenetic silencing. NeoDarwinian theory reasoned that by comparing the TSDs of non-autonomous TEs in different species they could infer common ancestry.  If two species have the same non-autonomous TE with the same TSD, then it was thought that this TE inserted into the genome of their common ancestor.

However epigenetics has challenged this. Different TEs use different epigenetic mechanisms to regulate TSD. Epigenetics controls TSD not simply an active autonomous TE. Therefore inferences about common ancestry are muted. This is because similar epigenetic mechanisms across all of life could lead to similar TSMs, even in organisms that are not closely related. Additionally, as epigenetics is guided by the environment, then common TSMs could represent common environments, rather than common ancestry.

Non-autonomous TEs can have a number of different effects on the genome. While non-autonomous TEs can be harmful, epigenetics can guide them to be beneficial. For example, they can help to create new genes and diversify the genome. They can also play a role in gene regulation and development.

Nonautonomous TE mobilization by epigenetics is very site-specific. This is because epigenetic modifications, such as DNA methylation and histone modifications, can be targeted to specific genomic regions. For example, in plants, the RNA-directed DNA methylation (RdDM) pathway can be used to target DNA methylation to specific TEs. In animals, PIWI-interacting RNAs (piRNAs) can be used to target DNA methylation and histone modifications to specific TEs.

The site-specificity of epigenetic TE mobilization is important because it allows the host cell to silence specific TEs without affecting the expression of nearby genes. For example, in humans, the L1 retrotransposon is silenced by DNA methylation in most somatic cells. However, L1 retrotransposition is reactivated in some cancer cells, which can contribute to tumorigenesis.

To recap before the discovery of epigenetics and "functional" Junk DNA, nonautonomous TEs were thought to be immobile "fossils" little useful except to claim common ancestry. 

With epigenetics it is now very difficult to conclude common ancestry because non-autonomous TEs can be mobilized and inserted into new locations in the genome, even if they are derived from different ancestral TEs. This can lead to a pattern of shared insertion sites between unrelated genomes, which could be misinterpreted as evidence of common ancestry.

For example, imagine that two species share a non-autonomous TE that is mobilized by epigenetics. If this non-autonomous TE is inserted into the same location in the genome of both species, it could be misinterpreted as evidence that the two species share a common ancestor. However, it is probable that the non-autonomous TE were independently mobilized in both species, and that the two species do not actually share a common ancestor.

The discovery of epigenetic mobilization of TEs has revolutionized our understanding of these elements and their role in genome adaptation.

At the same time it has negated the idea TEs are Junk DNA useful only for common ancestry.

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