CYP51A1 upstream anomalies and overexpression in myclobutanil and difenoconazole resistant Venturia inaequalis isolates
S. VILLANI (1), K. Cox (1). (1) Cornell University, Geneva, NY, U.S.A.
Upstream insertions of genetic elements and subsequent overexpression of the <i>CYP51A1</i> gene were previously found to promote resistance to myclobutanil in populations of <i>Venturia inaequalis</i> from Michigan. Adoption of DMI fungicides with different levels of intrinsic activity in apple scab management programs necessitates a reexamination of <i>CYP51A1</i> expression in isolates with varying DMI sensitivity phenotypes. 36 <i>V. inaequalis</i> isolates with ranges in sensitivity to myclobutanil and difenoconazole (0.1 μg/ml) were collected from a NY state research and baseline orchard and analyzed for <i>CYP51A1</i> upstream anomalies and expression. Amplification upstream of <i>CYP51A1</i> identified 2 novel insertions of 352bp and 183bp, and 2 previously documented insertions of 499bp and 224bp. Within the insertions, 4 different promoters were identified, but were not associated with resistance to either fungicide. Additionally, several isolates with resistance to difenoconazole, but not myclobutanil, had insertions of 5kb or 8kb in length located 149bp upstream of the <i>CYP51A1</i> start codon. <i>CYP51A1</i> expression was evaluated for all isolates using qRT-PCR. While relative <i>CYP51A1</i> expression of difenoconazole-sensitive isolates was significantly lower than difenoconazole-resistant isolates, there was no relationship between myclobutanil sensitivity and <i>CYP51A1</i> expression. The results suggest a lack of DMI cross resistance in <i>V. inaequalis</i> and involvement of different mechanisms of resistance.
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