IDPs and it's Prions acts outside of the Central Dogma of evolution

Epigenetics is the study of changes in gene expression that are not caused by changes in the DNA sequence as per NeoDarwinism. These changes can be inherited from one generation to the next, and they can affect how genes are turned on and off.

IDPs (intrinsically disordered proteins) are proteins that lack a well-defined three-dimensional structure. They are often involved in signaling and regulatory pathways, and they can be affected by epigenetic changes.


Beneficial prions are epigenetically folded IDPs. Bad prions are structured proteins that become  infectious agents. They can cause neurodegenerative diseases such as Creutzfeldt-Jakob disease and bovine spongiform encephalopathy (BSE).

Prions are a unique type of agent. They are not made of DNA or RNA, but they are able to spread from one cell to another by converting other proteins into prions. IDP/prions can cause phenotype adaptation outside of the Central Dogma of NeoDarwinism for thousands of generations. 

IDPs can take on prion configurations for phenotypic inheritance outside of DNA. In fact, this is a well-studied phenomenon in yeast, where prions have been shown to be a common mechanism for phenotypic inheritance.

IDPs are a type of protein that is unstructured or partially structured. This means that they can adopt a variety of different conformations, depending on their environment. This makes them capable for  prion formation, as they can easily fold into a prion-like conformation.

Once a IDP has folded into a prion-like conformation, it can then act as a template for other IDPs to fold in the same way. This can lead to the inheritance of a particular phenotype, even though the DNA sequence of the organism has not changed per NeoDarwinism.

Prions have been shown to be involved in a variety of epigenetic phenotypic traits in yeast, including mating type, sporulation, and resistance to stress. They are also thought to play a role in the Lamarckian evolution of new traits in yeast. Research has also shown they can form the scaffolding of brain cells. 

Prions can cause epigenetic phenotypic inheritance for thousands of generations outside of the DNA. This violates the central dogma of molecular biology, which states that genetic information is only passed from DNA to RNA to protein.


 In the case of prions, the information is encoded in the folding of the protein itself, and this information can be passed on to subsequent generations of proteins.


There is evidence that prions can be inherited for thousands of generations. For example, one study found that prions could be passed on for up to 1,500 generations in yeast. This suggests that prions could play a role in the Lamarckian evolution of new traits.

The discovery of prions has challenged our understanding of the central dogma of molecular biology. It has shown that protein information can be passed on in ways that do not involve DNA. This could have important implications for our understanding of how adaptation works as well as rethinking Darwinian evolution.

In the case of IDPs, epigenetic changes can alter the folding of the protein, making it more likely to form a prion. This can happen through a variety of mechanisms, including changes in the protein's post-translational modifications, such as phosphorylation or methylation.

Once a prion has formed, it can be transmitted to other cells, either through contact or through the environment. The prion can then cause the other cells to fold into their conformation, creating a chain reaction.

This process of epigenetic inheritance of prions can last for thousands of generations, outside of the DNA. This is because prions can be transmitted through the cytoplasm, which is not affected by DNA replication.

In the case of prions, the information is encoded in the protein's folding pattern. This information can be transmitted to other cells through contact or through the environment, even if the DNA does not change.


The main difference between prions and other IDPs is that prions can self-propagate. This means that a prion from a structured protein can induce a normal protein to fold into the prion's abnormal shape. This can lead to the formation of a prion aggregate, which is a large clump of misfolded prion proteins. Prion aggregates can damage brain cells and eventually lead to prion disease.

In addition to regulating the expression of genes, epigenetics can also influence the folding of IDPs and prions. For example, DNA methylation can alter the folding of IDPs, making them more or less likely to fold. This can affect the ability of IDPs to interact with other proteins and regulate gene expression.

Epigenetic regulation of IDPs and prions can play a role in adaptation to environmental changes. For example, exposure to certain chemicals can induce DNA methylation, which can lead to changes in the expression of genes that encode IDPs and prions. This can in turn lead to changes in the phenotype of the organism, which can help it to adapt to the new environment.

Studies suggest that epigenetics is a powerful force that can shape the phenotype of cells and organisms. It is an area of active research, and there is still much that we do not know about how it works. However, the potential implications of epigenetic inheritance for human health and evolution are significant.

Here are some additional resources that you may find helpful:

  • Prions and the Inheritance of Environmentally Acquired Traits

  • Prions are a common mechanism for phenotypic inheritance in wild yeasts

  • More than just a phase prions at the crossroads of epigenetic inheritance and evolutionary change

  • Familial Prion Disease


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