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Keywords:

  • demethylation-inhibitors;
  • quinone-outside-inhibitors;
  • overexpression;
  • point mutation;
  • sterol 14α-demethylase;
  • cyp51;
  • cytochrome b;
  • Phakopsora pachyrhizi;
  • soybean rust

Abstract

BACKGROUND

Since the invasion of Phakopsora pachyrhizi (Syd. & P. Syd.) in Brazil, there have been detrimental yield losses of soybeans [Glycine max (L.) Merr.]. Disease management is mainly based on fungicide treatment. The sensitivity of single P. pachyhrizi isolates towards different demethylation-inhibitors (DMIs) and quinone-outside-inhibitors (QoI) was surveyed and the corresponding resistance mechanisms were analysed.

RESULTS

The QoI-response remained stable, while a loss of sensitivity towards DMIs occurred. Molecular analyses of cytochrome b showed an intron after codon 143 which is reported to prevent the development of a G143A mutation. Analysis of cyp51 revealed that point mutations and overexpression are involved in the sensitivity reduction towards DMIs. Of the detected mutations, Y131F and Y131H, respectively, and K142R are likely homologous to mutations found in other pathogens. As suggested by modelling studies, these three mutations as well as additional mutations F120L, I145F and I475T correlate to increased effective doses of 50%, ED50-values, towards all tested DMIs. Furthermore, a constitutive up-regulation of the cyp51-gene up to ten-fold was noticed in some of the DMI-adapted isolates, while all sensitive isolates responded as the wild type.

CONCLUSION

The G143A mutation is thought to result in significant as well as stable resistance factors towards QoIs, while other mutations play only a minor role. Since G143A development is prevented in Phakopsora pachyhrizi, a stable control of soybean rust with QoIs in future is rather likely. In contrast, a shifting in sensitivity towards DMIs has been observed, which is due to multiple independent mechanisms. © 2013 Society of Chemical Industry