Clinically, a number of heritable immune disorders such as blood-cell related trait and rheumatoid arthritis are derived from critical proteins not synthesized or not functioning correctly. Nonetheless, the anatomy of regulation of an individual’s genes and how these resulting proteins interact to result in diseases is not widely known.
A new finding by researchers at University of Chicago, published in Nature Genetics, says N6 – Methyladenosine – a type of RNA chemical modification – plays an important role in heritability of human diseases.
The study of immune cells reveals that deformities in m6A levels may match with blood cell-related traits and autoimmune diseases. The understanding of this relationship is an opportunity to change the process and treat heritable human diseases.
New Approach addresses shortcomings of Earlier Techniques
“The topic is a modern one in the field of genetics. And, to study this, researchers employed a different approach than other studies,” stated the lead author of the paper.
Meanwhile, several studies focus on role of genetic variation in transcription, i.e.to turn DNA into messenger RNA. On the other hand, the study demonstrates involvement of genetic variation in m6A liaised post-transcription regulation such as converting messenger RNA into proteins.
Employing a statistical technique called QTL mapping, while mapping the analysis of m6A data, researchers found that m6A is as impactful to modulate disease susceptibility as it is for RNA splicing, and that it is half as impactful for gene expression.
With the study of mechanisms of m6A related to diseases, this could help researchers be one step closer to develop treatments for these diseases. Meanwhile, genetic modification to m6A could have the implication that mRNA is not translated into necessary proteins. For this, future therapies can aim this pathway to tune disease susceptible genes to the level of m6A.