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Targeting fungal RNA through the incorporation of fluorouracil exploits a vulnerability shared by all eukaryotes—the dependence on precise post-transcriptional modification and processing events. By substituting uridine residues with a non-canonical base throughout diverse classes of functional RNAs—including those essential for protein synthesis and gene expression regulation—this approach induces widespread dysfunction culminating in cell death. The mechanism involves not only direct interference with individual transcripts but also global impairment across multiple layers including splicing machinery integrity, ribosomal activity, transfer-RNA functionality, and nuclear surveillance systems.
Incorporation into nascent RNAs → defective modification/processing → functional impairment
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