Researchers have pinpointed a protein that regulates the information present in "ribonucleic acid molecules"; these molecules are responsible for transporting genetic information from DNA to protein synthesis.
The team found the protein ADR-1 attaches itself to mRNA and influences its "editing process," which determines where genes are expressed mRNAs, an Indiana University news release reported.
Decreased mRNA editing has been linked to neuropathological diseases such as schizophrenia, epilepsy, and even certain types of cancer.
Using the organism Caenorhabditis elegans, the team identified about 400 new mRNA editing sites, many of which were regulated by ADR-1.
"What we've determined is that this protein's ability to alter editing of mRNAs is not specific to just a few genes, but instead, its ability to bind to mRNAs is required for proper RNA editing of most mRNAs," Michael C. Washburn, a graduate student in the IU College of Arts and Sciences' Department of Biology, said in the news release.
The team determined the region of ADR-1 that binds to specific mRNAs in C. elegans are required for regulation. A protein similar to ADR-1 is expressed in human neurons.
"So it is likely that a similar mechanism exists to regulate editing in humans," Heather A. Hundley, corresponding author on the paper and an assistant professor of biochemistry and molecular biology in the IU School of Medicine's Medical Sciences Program said in the news release. "Further work in our lab will be aimed at understanding the detailed mechanism of how these proteins regulate editing, in turn providing an inroad to developing therapeutics that modulate editing for the treatment of human diseases."
C. elegans is a microscopic work that "like humans highly expresses a family of proteins in the nervous system called ADARs," the news release reported.
ADARs are responsible for influencing specific nucleotides ("building blocks of DNA and RNA) in a process that "diversifies genetic information to specify different amino acids, splice sites and structures," the news release reported.
"One thing we also know is that ADAR protein levels are not altered in disease, implying that other mechanisms are also at work regulating ADAR-mediated RNA editing," Hundley said. "By identifying this major regulator of noncoding editing in C. elegans we can now focus on dissecting the regulatory mechanism and determining the conservation of this regulatory protein in human cells."
