Genetic structure and fungicide sensitivity of the population of Sclerotinia sclerotiorum in Brazil

Detalhes bibliográficos
Ano de defesa: 2018
Autor(a) principal: Silva, Rhaphael Alves
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: eng
Instituição de defesa: Universidade Federal de Viçosa
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://www.locus.ufv.br/handle/123456789/21851
Resumo: Sclerotinia sclerotiorum causes white mold or sclerotinia stem rot and affects important crops such as grains, fibers and vegetables. This study was conducted to assess the genetic variability; the sensitivity to thiophanate-methyl (TM), fluazinam and procymidone of 238 isolates of S. sclerotiorum from different hosts and regions in Brazil; and the phenotypic stability of fungicide resistant isolates. Microsatellites (SSR) and mycelium compatibility groups (MCG) markers were used to assess the genetic structure of the population. Twenty-two MCGs and 53 multilocus genotypes (MLG) were identified. Most isolates (67.7 %) were distributed in either MCG 1 or 2. Seven genetic groups were detected. The population has a clonal structure largely determined by MCGs and there was no evidence of random mating. Fungicide sensitivity was assessed using the discriminatory doses for TM, fluazinam and procymidone. The stability of nine isolates TM-resistant and one sensitive was assessed after 10 transfers in culture medium without fungicide. Mycelial growth rate of six TM-resistant isolates reduced with successive transfers. There was no evidence of resistance to fluazinam or procymidone. Thirteen isolates collected in common bean fields in the municipalities of Cabeceira Grande (8 isolates) and Unaí (5 isolates), Minas Gerais state, were resistant to TM. The resistance was associated with the L240F mutation in the β-tubulin gene. Resistance to TM seems to be localized; and there is evidence for a fitness cost in resistant isolates.