Abstract
RNA interference (RNAi) was discovered at the end of last millennium, changing the way scientists understood regulation of gene expression. Within the following two decades, a variety of different RNAi mechanisms were found in eukaryotes, reflecting the evolutive diversity that RNAi entails. The essential silencing mechanism consists of an RNase III enzyme called Dicer that cleaves double-stranded RNA (dsRNA) generating small interfering RNAs (siRNAs), a hallmark of RNAi. These siRNAs are loaded into the RNA-induced silencing complex (RISC) triggering the cleavage of complementary messenger RNAs by the Argonaute protein, the main component of the complex. Consequently, the expression of target genes is silenced. This mechanism has been thoroughly studied in fungi due to their proximity to the animal phylum and the conservation of the RNAi mechanism from lower to higher eukaryotes. However, the role and even the presence of RNAi differ across the fungal kingdom, as it has evolved adapting to the particularities and needs of each species. Fungi have exploited RNAi to regulate a variety of cell activities as different as defense against exogenous and potentially harmful DNA, genome integrity, development, drug tolerance, or virulence. This pathway has offered versatility to fungi through evolution, favoring the enormous diversity this kingdom comprises.
Highlights
RNA interference (RNAi) or RNA silencing has been deeply studied in the last two decades, as its discovery entailed a revolution in the understanding of the regulation of gene expression
This RNAi pathway, broadly conserved in eukaryotes (Table 1), uses small interfering RNAs to suppress gene expression of homologous sequences. These siRNAs, of 20–30 nucleotides long, are produced from double-stranded RNA by an RNase III called Dicer (Dcr) and loaded into an RNA-induced silencing complex (RISC), which contains an Argonaute protein (Ago) that drives the selective degradation of homologous messenger RNAs, as well as translational or transcriptional repression of target sequences
RNAi drives virus inactivation through the production of virus-derived small interfering RNAs originated from viral double-stranded RNA (dsRNA) [70]. This RNAi-based mechanism has been widely explored in the ascomycete filamentous fungus Cryphonectria parasitica, which is considered a model for the analysis of virus–fungus interactions because it can be infected by five different virus families
Summary
RNA interference (RNAi) or RNA silencing has been deeply studied in the last two decades, as its discovery entailed a revolution in the understanding of the regulation of gene expression. This RNAi pathway, broadly conserved in eukaryotes (Table 1), uses small interfering RNAs (siRNAs) to suppress gene expression of homologous sequences. These siRNAs, of 20–30 nucleotides (nt) long, are produced from double-stranded RNA (dsRNA) by an RNase III called Dicer (Dcr) and loaded into an RNA-induced silencing complex (RISC), which contains an Argonaute protein (Ago) that drives the selective degradation of homologous messenger RNAs (mRNA), as well as translational or transcriptional repression of target sequences. In fungi and other organisms, an RNA-dependent RNA polymerase (Rdp or RdRP) generates dsRNA from certain single-stranded RNA (ssRNA) or from the target messenger RNA, activating or amplifying the silencing response, respectively [1,2]
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