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The fungal RNA interference (RNAi) pathway encompasses diverse mechanisms for small RNA (sRNA) biogenesis and function, primarily involving core components Dicer (RNase-III enzyme cleaving dsRNA into 21-25 nt siRNAs or miRNAs), Argonaute (in RISC complex for target mRNA slicing or repression), and RNA-dependent RNA polymerase (RdRP, amplifying dsRNA from aberrant RNA). In species like Neurospora crassa and Schizosaccharomyces pombe, it mediates genomic defense against transgenes or viruses (quelling), heterochromatin formation at centromeres and rDNA loci via H3K9 methylation, DNA damage checkpoints by inhibiting protein synthesis, and meiotic silencing of unpaired DNA. These pathways often start with aberrant RNA or ssDNA templates producing antisense RNA (aRNA) via dual DdRP/RdRP activity, processed into sRNAs for gene silencing. In plant-pathogenic fungi like Botrytis cinerea, exogenous dsRNA is taken up, triggering RNAi to downregulate essential genes such as those in ergosterol biosynthesis, inhibiting growth and infection. This positions fungal RNAi as a promising antifungal target, exemplified by topical dsRNA sprays reducing postharvest grey mold decay without broad toxicity.
RNA interference (processing dsRNA into siRNA/miRNA by Dicer, loading into Argonaute-containing RISC for mRNA cleavage or translational repression; aberrant RNA conversion to dsRNA by RdRP; aRNA production from ssDNA by DdRP activity)
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