RNA Editing of Genomic Neighbors Controls Antiviral Response in Fungi

Viruses that weaken pathogenic fungi and reduce their virulence are being considered as biological control agents. However, the mechanism behind viral symptom expression is not fully understood, partly due to the unidentified genes involved. Here, we used Neurospora crassa, a newly established model of fungal virology to demonstrate that ribonucleic acid (RNA) editing controls the antiviral response. The player genes comprised two pairs of adjacent genes in the genome, one being an A-to-I RNA editing enzyme, OTT_1508-like deaminase (old), and the other being its target, zinc fingers adjacent to old (zao), which controls all transcriptional responses to viral infection. High levels of RNA-edited zao-1/2 mRNAs induce excessive antiviral responses, resulting in growth defects, while proper levels induce normal antiviral responses, leading to asymptomatic viral infection. The major filamentous fungi were shown to possess homologs as genomic neighbors, indicating that this RNA editing system is an evolutionarily conserved antiviral mechanism.