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Characterization of difenoconazole resistance in Lasiodiplodia theobromae from papaya in Brazil.

BACKGROUND
Stem-end rot caused by Lasiodiplodia theobromae is one of the most important diseases of papaya in northeastern Brazil. It can be controlled effectively by demethylation inhibitor (DMI) fungicides, but occurrence of DMI resistance may decrease fungicide efficacy.


RESULTS
Detached fruit studies revealed that isolates with EC50 values of 6.07 and 6.28 μg/mL were not controlled effectively, but reduced virulence and reduced ability to grow at temperatures ranging from 12 to 32 °C suggesting fitness penalties were observed. Cross-resistance was observed only between difenoconazole and propiconazole. The entire cytochrome P450 sterol 14α-demethylase (LtCYP51) gene and its flanking regions were cloned. The gene was 1746 bp in length and contained three introns. The predicted protein contained 525 amino acids. Phylogenetic tree analysis showed that the LtCYP51 belongs to the CYP51B clade. No amino acid variation was found between sensitive and resistant isolates, however, the gene was constitutively higher expressed in resistant isolates.


CONCLUSION
Resistance to DMI fungicides in L. theobromae is based on LtCYP51 gene overexpression and fitness penalties may be present in difenoconazole resistant isolates. This article is protected by copyright. All rights reserved.