The genetics of the responses of the barley powdery mildew pathogen, Erysiphe graminis f.sp. hordei, to three morpholine-type fungicides were studied. Resistances to a phenylpropylamine fungicide, fenpropidin, and to a morpholine, fenpropimorph, co-segregated in crosses of a sensitive isolate, DH14, with each of two resistant ones, CC151 and CC152. In the cross CC151 x DH14, the results were consistent with resistance to both fungicides being controlled by a single gene, at a locus named Fen1. In the other cross, CC152 x DH14, the genetics of resistance were more complicated; the data were cons;stent with the segregation of two complementary, unlinked genes which each conferred resistance to both fungicides. Fenpropidin-resistant progeny of CC151 x DH14 were significantly more resistant to fenpropimorph than were fenpropidin-resistant progeny of CC152 x DH14, although the resistant progeny of the two crosses did not differ significantly in their level of fenpropidin resistance. Fenpropidin-resistant progeny of CC151 x DH14 were significantly more resistant to another morpholine, tridemorph, than were fenpropidin-sensitive progeny, but this was not the case for CC152 x DH14. Resistance to triadimenol a C14 demethylation-inhibitor (DMI) fungicide, segregated in both crosses. Triadimenol resistance appeared to be controlled by one gene in each cross and was not associated with morpholine resistance. CC151 x DH14 also segregated for eight avirulence genes. Two of these matched the Mla6 resistance, while one gene matched a previously unknown resistance in a Pallas near-isogenic line, P17, which also carries a known resistance gene, MlK Fenl was not significantly linked to the triadimenol resistance gene, Tdl(a), or to any of the eight avirulence genes. Avr(a6)l, Avr(a12), AVr(La), Avr(P17) and Tdl(a) were linked, as were Avr(a10) to and Avr(k).