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Genetics

Genetic Correlations in Resistance to Sterol Biosynthesis-Inhibiting Fungicides in Pyrenophora teres. Tobin L. Peever, Department of Plant Pathology, Cornell University, Ithaca, NY 14853; Michael G. Milgroom, Department of Plant Pathology, Cornell University, Ithaca, NY 14853. Phytopathology 83:1076-1082. Accepted for publication 25 June 1993. Copyright 1993 The American Phytopathological Society. DOI: 10.1094/Phyto-83-1076.

We investigated cross-resistance in Pyrenophora teres to five sterol biosynthesis-inhibiting fungicides (SBIs) by calculating genetic correlations in resistance. Two approaches were used in separate experiments to estimate the correlations: In one method, progeny sampled from crosses of P. teres were used to determine "among-family" genetic correlations; in the other method, replicated isolates sampled from different P. teres populations were used to calculate "among-isolate" genetic correlations. Resistances to some members of the demethylation inhibitor (DMI) group of SBIs (triadimenol, propiconazole, imazalil, and fenarimol) were highly genetically correlated in both experiments, consistent with the hypothesis that many of the same genes, or genes in gametic disequilibrium, control resistance to these DMIs. However, resistances to several other pairs of DMIs had correlation coefficients that were not significantly different from zero, indicating that independent genes may control resistance to these pairs. Genetic correlations in resistance to DMIs and the morpholine SBI fenpropimorph appeared to differ from the DMI-DMI correlations, and many of the coefficients were not significantly different from zero, consistent with the hypothesis that independent genes control resistance to DMIs and fenpropimorph. Some of the genetic correlation coefficients in resistance to DMIs and fenpropimorph, however, were not significantly different from one, indicating that in certain P. teres populations, the same genes or genes in gametic disequilibrium controlled resistance to these pairs of SBIs. Many of the correlation coefficients in resistance to any given pair of SBIs differed among populations of P. teres, indicating significant genetic differentiation among these populations. The variability in correlation coefficients observed between DMI-DMI and DMI-fenpropimorph combinations and among populations indicates that no single model of cross-resistance among SBIs and among all P. teres populations is appropriate. Among-isolate genetic correlations provided more accurate estimates of cross-resistance among SBIs than the among-family estimates and represent the most evolutionarily relevant approach to studying genetic correlations in resistance in P. teres and other predominantly asexually reproducing fungi.