Identification and Characterization of Inherent Resistance to 14α-demethylation Inhibitors in Colletotrichun truncatum
Shuning Chen: Institute of Plant Protection, Chinese Academy of Agricultureal Sciences
<div>Anthracnose disease caused by<em> Colletotrichum truncatum</em> is a major economic constraint to fruits and vegetables in the tropical and subtropical regions of the world. Isolates of <em>C. truncatum</em> were collected from the US and China from peach, soybean, and citrus and their sensitivity to demethylation inhibitor fungicides (DMIs) including difenconazole, propiconazole, tebuconazole, metconazole, flutriafol, and fenbuconazole was determined. In contrast to <em>Colletotrichum fructicola, Colletotrichum siamense, </em>and <em>Colletotrichum fioriniae </em>isolates<em>, </em>all <em>C. truncatum</em> isolates were resistant to tebuconazole, metconazole, flutriafol, and fenbuconazole, and less sensitive to difenconazole and propiconazole. The <em>Colletotrichum</em> spp. genome contained two homologous <em>CYP51</em> genes, <em>CYP51A</em> and <em>CYP51B</em> that putatively encode sterol 14α-demethylase enzymes. The <em>CYP51A</em> and <em>CYP51B</em> from <em>C. truncatum</em> and other species were cloned to investigate the molecular basis of inherent resistance to DMI fungicides in <em>C. truncatum</em>. Quantitative expression analysis did not show correlations between the<em> CYP51 </em>expression level and fungicides senstitivity. Amino acid sequences were compared among different <em>Colletotrichum </em>species within substrate recognition sites. Four amino acid variations L208Y, H238R, S302A, I366L from <em>CYP51A</em>, and three variations H373N, M376L, S511T from <em>CYP51B</em> correlated with the DMI resistance phenotype. Molecular docking with<em> CYP51A</em> structure models suggested the four variations in <em>CYP51A</em> reduce azoles interactions with critical residues in the binding cavity, thereby causing inherent reistance to DMI fungicides in <em>C. truncatum</em>.</div>
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