Junk DNA (TEs), ncRNAs plus IDPs challenges NeoDarwinism

"In terms of Junk DNA, we don’t use that term anymore because I think it was pretty much a case of hubris to imagine that we could dispense with any part of the genome, as if we knew enough to say it wasn’t functional. … Most of the genome that we used to think was there for spacer turns out to be doing stuff.”- Francis Collins, head of the Human Genome Project (HGP)


Transposable elements (TEs), also known as "jumping genes," were once thought to be "Junk DNA", but we now know that they play an important role in gene regulation and NonDarwinian evolution. They make up 98% of our DNA. 

The Human Genome Project (HGP) (above) assumed that TEs were Junk DNA, and this contributed to the project's failure to fully achieve its goals. Because of this the HGP did not identify all of the genes in the human genome, and it did not fully explain how genes are regulated. The study cost 7 billion dollar and took 11 years to complete only to be a dud by ignoring 98% of the DNA due to NeoDarwinian thinking.

The ENCODE project, with 400 labs and thousands of scientists, which followed the HGP, disproved the idea that TEs are junk DNA and showed that they play a major role in regulating the expression of our genes. 98% of TEs are within 1,000 base pairs of our genes. As such they regulate the genome. (video)

The term "junk DNA" was also errantly used to support the idea of common ancestry. Scientists thought they were nonfunctional fossils. We've now discovered that Junk DNA moves are functional and are controlled by NonDarwinian epigenetics makes common ancestry  phylogenetic comparisons problematic.


Recent studies have shown that TEs are a major source of noncoding RNA (ncRNA). NcRNAs are RNA molecules that are not translated into proteins. NeoDarwinism only takes into account coding polymers. NcRNA play a variety of important roles in gene regulation, including chromatin modification, RNA splicing, and microRNA (miRNA) biogenesis.

It is estimated that up to 80% of all ncRNAs in humans are derived from TEs. This includes a wide variety of ncRNA types, including small interfering RNAs (siRNAs), miRNAs, long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs).

Types of noncoding RNA from TEs

Small interfering RNAs (siRNAs) are short double-stranded RNA molecules that can silence gene expression. SiRNAs can be derived from TEs through a process called RNA interference (RNAi). RNAi is a powerful gene regulatory mechanism that is found in all eukaryotes.

MicroRNAs (miRNAs) are another type of short noncoding RNA that can regulate gene expression. MiRNAs bind to the 3' untranslated regions (UTRs) of target mRNAs and either promote their degradation or repress their translation. MiRNAs can also be derived from TEs through RNAi.

Long noncoding RNAs (lncRNAs) are noncoding RNA transcripts that are longer than 200 nucleotides. LncRNAs play a variety of roles in gene regulation, including chromatin modification, RNA splicing, and miRNA biogenesis. Many lncRNAs are derived from TEs.

Circular RNAs (circRNAs) are a type of noncoding RNA that is formed by a backsplicing event. CircRNAs are more stable than linear RNAs and can play a role in gene regulation. CircRNAs can also be derived from TEs.

Overall, noncoding RNAs from TEs are a diverse and important class of RNA molecules that play a variety of roles in gene regulation.


IDPs are proteins that lack a well-defined three-dimensional structure. They are often found in signaling and regulatory proteins, where their disordered nature allows them to interact with multiple different partners. IDPs are also very common in eukaryotes, where they make up about 40% of all proteins. In humans they make up the majority (51%) of proteins. We also know most of our structured proteins have some intrinsic disorder.

Intrinsically disordered proteins (IDPs) defy NeoDarwinism because they can sustain more mutations over billions of years with no change in function. This defeats gradualism, the NeoDarwinian view that evolution is a slow and gradual process driven by the accumulation of small mutations. IDPs are in essence in evolutionary stasis, meaning that they do not evolve over time. IDPs function does not depend on a specific three-dimensional structure. As a result, IDPs can accumulate many mutations over time without losing their function. This makes them very different from other structural proteins, which are typically very sensitive to mutations.

The fact that IDPs can sustain many mutations without losing their function has important implications for our understanding of non darwinian evolution. It means that IDPs can remain in evolutionary stasis for billions of years. This is in stark contrast to the NeoDarwinian view that evolution is a slow and gradual process driven by the accumulation of small mutations.

The fact that IDPs are so common and tolerant of mutations means that they play a significant role in NonDarwinian evolutionary stasis. This suggests that the theory of NeoDarwinian evolution needs replacement as the majority of proteins are IDPs not structural proteins.

The percentage of TE's genes that code for intrinsically disordered proteins (IDPs) varies depending on the type of TE. However, in general, TEs have a higher percentage of IDP-coding genes than non-TE genes.

For example, a study of human TEs found that 51% of TE-encoded proteins are IDPs, compared to 25% of non-TE-encoded proteins. Another study found that 30% of maize TE-encoded proteins are IDPs, compared to 15% of non-TE-encoded proteins. IDPs are often more efficient at binding to other proteins and nucleic acids, which can be advantageous for TEs that need to interact with other genetic elements in order to move around the genome.

IDPs play a variety of roles in TE function. For example, IDPs can be involved in the regulation of TE transcription, the formation of TE complexes, and the movement of TEs to new locations in the genome.

Overall, TEs have a higher percentage of IDP-coding genes than non-TE genes.

Per theory, Natural selection can only work on proteins with a fixed structure because natural selection acts on the phenotype of an organism, which is determined by the proteins that are expressed in the organism. 


In order for a protein to have a fixed structure, it must have a specific sequence of amino acids. Mutations that change the amino acid sequence of a protein can also change its structure and function. If a mutation changes the structure of a protein in a way that makes it less functional, then the organism is less likely to survive and reproduce. If the mutation improves the structure per theory they are selected for (natural selection). During the last half of the last century scientists were largely only aware of structured proteins. Subsequently they applied NeoDarwinism to them in what's called the "sequence structure hypothesis." This is why natural selection was though to only act on proteins with a fixed structure.

In 1999, a landmark article by Dunker and colleagues provided the first comprehensive analysis of IDP prevalence and function. This article helped to establish IDPs as a legitimate and important area of research.

It is thought that IDPs are not under natural selection because they do not have a fixed structure. This means that they are able to interact with a variety of other proteins and molecules without having to undergo a large conformational change. This flexibility is essential for many of the functions that IDPs perform. There are many ways that IDPs can be functionally important even though they are not under natural selection due to not having a fixed structure.

In conclusion the vast majority of organisms DNA in TEs (98%) and genes for coding IDPs are not under natural selection. The remaining 1% of exons that remain are controlled by epigenetics which further obscures natural selection.

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