Transmission of the G143A QoI‐resistance point mutation through anastomosis in Magnaporthe grisea

Abstract

Soon after the introduction of Qo inhibitor fungicides in 1996, the point mutation leading to the amino acid exchange glycine to alanine at the 143 position of the mitochondrial cytochrome b gene was identified as the main cause of resistance. The present study describes the role of anastomosis in the transmission of the G143A mutation in Magnaporthe grisea. Two M. grisea mutants were co-cultivated on oatmeal agar and also co-inoculated on barley leaves. The mutants differed by the presence of the G143A mutation in one isolate and a disrupted AOX gene by insertion of a hygromycin gene in the other (M-145). Specific resistant (r) or sensitive (s) phenotypes of 409 monosporic cultures were determined on media amended with either hygromycin (H) or azoxystrobin (S) plus SHAM. The phenotypes identified reflected not only the phenotypes of mutants M-145 and G143A but also the wild-type parent phenotype HsSs and a new HrSr isolate. Identification of the M. grisea phenotypes HrSr and HsSs suggests that anastomosis occurred during co-cultivation and co-inoculation of the mutants M-145 and G143A, allowing the transfer of the G143A point mutation from the QoI-resistant isolate to the susceptible isolate.