Fungi - Candida albicans - Research News, Data, Publications & Aproaches - ERG11 Mutations - Telomeres - Sub-Telomeric Structures - Nuclear Biology & Nuclear Chemistry Aproaches - The Evolutionary Logic of Telomeric Embedding of ERG11 - Non-Elaborate Posts - Post 4
This “evolutionary incubator” model becomes even more compelling when considering the interplay between ERG11 and antifungal selection. Azole drugs, which target the heme-binding pocket of lanosterol 14α-demethylase, apply strong directional pressure that favors mutations attenuating drug interaction while preserving enzymatic efficacy. Telomere-proximal DNA fosters precisely these modifications by virtue of its recombination-prone architecture. Mutations such as Y132F or K143R arise with greater frequency in subtelomeric sequences due to increased replication stress, impaired telomere maintenance, or chromatin compaction cycles. Therefore, the location of ERG11 is not a vulnerability but an adaptive scaffold enabling selective, incremental refinement of azole resistance phenotypes.
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