Yuan Li1, Susan Satie Tsuji2, Mengjun Hu3, Marcos Paz Saraiva Câmara2, Sami Jorge Michereff4, Guido Schnabel5, Fengping Chen1. 1. Department of Plant Pathology, Fujian Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University, Fuzhou, China. 2. Departamento de Agronomia, Universidade Federal Rural de Pernambuco, Recife, PE, Brazil. 3. Department of Plant Science and Landscape Architecture, University of Maryland, College Park, MD, USA. 4. Centro de Ciências Agrárias e da Biodiversidade, Universidade Federal do Cariri, Crato, CE, Brazil. 5. Plant & Environmental Sciences, Clemson University, Clemson, SC, USA.
Abstract
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 the 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-1 were not controlled effectively, but reduced virulence and 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 more highly 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.
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 the 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-1 were not controlled effectively, but reduced virulence and 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 more highly 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.
Authors: Jadran F Garcia; Daniel P Lawrence; Abraham Morales-Cruz; Renaud Travadon; Andrea Minio; Rufina Hernandez-Martinez; Philippe E Rolshausen; Kendra Baumgartner; Dario Cantu Journal: Front Microbiol Date: 2021-03-18 Impact factor: 5.640