Photo: Molecules, wastedgeneration, Pixabay
A tiny insertion of a highly charged, binding potential helix into the space of RNA after the prokaryote code was lost or removed could change the direction of life’s evolution.
RNA is a single-strand of ribonucleic acid, which is more primordial to DNA built with two strands and slightly different bases. It could be RNA that assembled the first pieces of life out of the prebiotic soup at the ancient Earth. Then it could transform into the more complex structure, which has been recognized as the original base for further evolution. However, the two structures still coexist in bodies in every life. Now, scientists of the Broad Institute of MIT and Harvard, in the last study published in ,,Cell”, claim that RNA may be reprogrammed to enable changes in the strength of the binding regions, guiding to both a slight loss of an original sequence of fast-moving alkalies and the gain of a new sequence transforming more than half of the original ancestor code within the strand.
What is elusive, what is persistent in the genome?
How is this possible that an action based on a primitive organism that, whether we like it or not, is in the majority on our planet, unleashes changes that might be key for modern medicine? This is possible due to an evolutionary mechanism called CRISPR, which subsists only with eukaryote organisms, while prokaryotes were the prior. The main difference between the two groups is the way of genetic material protection. Concerning prokaryotes, it is located in separate chromosomes and plasmids. In the case of eukaryotes, the genetic code gathered from the progenitor is located in the nucleus of the cell. Simplifying the CRISPR mechanism that is currently crucial for our disease susceptibility/resilience, cuts off a portion of the original version of the code in selected loci (locations). But, what’s awesome and discovered by the scientists, the transforming RNA is acquiring a boost of energy with a highly charged duplex binding and thought the capability for a new dedicated amino. That compensation enables us to reach the final change and thus continue repeats. However, those are changing. And this is it, what alters the direction of the evolutionary mechanisms driving life-origin, at the same time, leaving the core genome without persistent changes.
What’s fascinating is that pieces of prokaryotic tracings remain in future RNA expressions and are found in non-coding RNA. These segments of the single strand do not bind to amino acids. Previously, some scientists referred to these sequences as “junk DNA,” believing they were not essential for the organism’s functioning, as amino acids trigger actions within the body. However, it is now clear that this so-called “junk” is quite stable and integral to cellular functions. Additionally, it is linked to the ability to eliminate unwanted infections. So, could it be that bacteria are crucial for our existence on Earth?
The origin of the RNA-targeting CRISPR-Cas13 and, more generally, the origin of RNA-guided targeting mechanisms in CRISPR systems have remained elusive,
claim Shai Zilberzwige-Tal and Feng Zhang of the Broad Institute of MIT and Harvard.
But, simultaneously, the structure being original for CRISP-Cas13 evolution is a toxin-antitoxin (TA) system with an RNA antitoxin – the scientists claim. The answer, what is our protection here might be more astonishing. A toxin called AbiF. Furthermore, characterization of the AbiF system revealed a distinct mechanism of action.
We discovered that Cas13 likely evolved from an abortive infection F (AbiF) protein associated with a non-coding RNA (ncRNA). AbiF is a toxin-antitoxin (TA) system with an RNA antitoxin,
say Shai Zilberzwige-Tal and Feng Zhang of the Broad Institute of MIT and Harvard.
In other words, unlike CRISPR, the relationship between the toxic protein and the non-coding RNA functions on a specific path, involving a reaction and an anti-reaction in the toxin-antitoxin system. The non-coding RNA can inhibit the active site of the AbiF nuclease, creating harmful effects while also introducing errors. The issue arises from a significant duplication of available binding sites, which consequently leads to the loss of interaction with the antitoxin encoded by certain non-coding RNAs. However, a new interaction with CRISPR RNA has emerged, facilitated by a small set of helical insertions and a single Recognition (REC)-like insertion in the effector protein. This modification likely enables the recognition of the duplex formed by guide RNA and target RNA, allowing the two complementary strands of RNA to function as part of a defense-related system linked to the AbiF toxin, according to the scientists’ conclusions.
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