Author: Anna Drhovská
Editor: Katie Kavanagh
Microbes play a crucial role in our lives, impacting them in both positive and negative ways. Apart from the occasional troubles the flu can cause us, we widely acknowledge the positive impact bacteria have on our lives, as they make up our gut microbiome or help us mass-produce insulin. Have you ever thought positively about viruses? The unexpected crossover of virology and neurology has just been uncovered with regard to the evolution of impulse transduction in vertebrates. Viral insertions in the past have served as a major switch in the formation of the myelin sheath, enabling saltatory movement of nerve impulses and helping them travel faster and more effectively. According to a research paper published by Cell Journal in February of this year, without them, you would not even be able to form complex thoughts as you are able to today.
The myelin sheath has long been the leading actor behind the mesmerising play of action potentials, signal transmission, and viability of the cells in the nervous system. It is an insulating layer of protein and fatty substances located around the fibre axons, enabling conduction at faster speeds without a significant increase in the cell diameter. It also causes the system of axons to be more dense and allows them to reach much further and form considerably more complex networks, contributing to the overall diversity and evolutionary advancement of vertebrate species. For decades, it has been observed in almost all classes of vertebrates, where it first originated in jawed species, and is generally acknowledged for its vital function in nerve support together with signal transduction. However, the mechanism of its origin was, up until now, a lingering shadow without any molecular clues about where to begin searching for its origin.
Scientists have recently shone light upon transposons and may be bearing the answer to the mysterious past of myelination. Transposomes, also known as Transposable Elements (TEs), are noncoding regions in our genome that not only makeup nearly 40% of our total genetic makeup but also exhibit a unique ability to reposition from one section of our genome to another. Hence, their general name is “jumping genes.” They can not only be transferred vertically, such as from mother to daughter cells during replication but also horizontally between non-replicating cells in our bodies and even between species. In eukaryotes, a significant subtype is the highly unique group of retrotransposons, which function by copying and pasting the new daughter DNA into a separate region from the stationary template. This February, researchers from Altos Labs-Cambridge Institute of Science have been observing the genes utilised by oligodendrocytes and progenitor cells to the myelin sheath in our central nervous system and came across an outstanding example of retrotransposon with an origin in viral insertion, coined RetroMyelin, originating from interactions with vertebrates.
Researchers have uncovered a mechanism in which the RNA transcript of the RetroMyelin transposon regulates the expression of one of the basic building blocks. Observations based on experiments with rodents revealed the regulation of myelin basic protein expression. With it inactivated, the oligodendrocytes could not synthesise the myelin basic protein, and the sheath did not form. With the study being later directed toward the search for RetroMyelin in other vertebrates, homologies were found across many diverse classes, including amphibians, fish, reptiles, and even birds. This implies that RetroMyelin as a transposon has had such an influence that it has been evolutionarily generalised and established with a generous set of vertebrates, including ourselves. The study has successfully proposed and also confirmed the importance of RetroMyelin for the formation of myelin sheath in zebrafish and frogs, thus showing us the light at the end of the tunnel in our search for evolutionary machinery standing behind the excellent intelligence surge we observe in ourselves.
The story of viral influence on our brains has not yet come to a halt, and researchers continue to write its script by attempting to harness their traits for the development of advanced therapies in neurological diseases, most prominently neuronal repair. A topic that has in recent days lured the attention of multiple academic groups worldwide is the use of viruses as vectors delivering material into the human nervous system, more specifically, in the majority of instances, tiny fragments of synthetic RNA to be inserted on-site into the targeted cells to induce repair in affected parts of the central nervous system. These natural “cargo containers” would provide future therapies with high specificity and vastly applicable manufacture, enabling people to regain control over their nervous system. For example, the use of viral vectors has tremendous implications in the treatment of Parkinson’s disease, as they ship enzymes deficient in the dopamine pathway straight to the core of the brain. In recent years, oncolytic viruses have emerged as a promising treatment for various types of brain cancer, including glioblastoma. These viruses are characterised by their ability to identify and destroy cancer cells while leaving normal cells unharmed.
Gradually, the evil aspects of viruses are being overshadowed by their potential benefits to our lives. While they continue to trouble many of us, we may eventually tame these invisible actors and integrate them into our bodies, reaping significant benefits much like the evolutionary developments that formed our myelin sheaths millions of years ago.
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