The virulence of a rice-wrecking fungus—and deployment of ninja-like proteins that help it escape detection by muffling an immune system's alarm bells—relies on genetic decoding quirks that could prove central to stopping it, says research from the University of Nebraska–Lincoln.
A Nebraska team helmed by Richard Wilson hopes that identifying an essential but formerly unknown stage in the fungal takeover of rice cells can accelerate the treatment or prevention of rice blast disease, which ruins up to 30% of global yields each year.
Before giving up their precious cargo, though, some tRNAs undergo chemical makeovers. One especially notable modification? The addition of sulfur to the tRNA's third letter, or nucleotide—specifically when that letter is U, the nucleotide known as uridine. Though that sulfur addition has been conserved and observed in a wide range of organisms, from yeast to mice to humans, researchers have yet to pin down all its functions.
That sulfur-modified tRNA could assist the search for disease-enabling effectors in M. oryzae and a rash of other pathogens, Wilson said. In the case of M. oryzae, tRNAs were consistently matching with mRNA codons ending in AA—adenine in the second and third positions of the codon. Yet the team knew that other tRNAs could also match with synonymous codons that instead ended in AG, unloading the very same amino acid when they did—and without the fuss of adding sulfur beforehand.
Because mRNA extracts its blueprints directly from the source code known as DNA, analyzing the latter can allow researchers to discern the presence and prevalence of codons in the former. Knowing just how heavily M. oryzae depends on AA-ending codons to churn out the effectors that invade a rice cell's cytoplasm, Wilson and his colleagues went looking for signs of them in relevant genes.
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