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Phenylpyrroles fungicides such as fludioxonil and dicarboximides such as iprodione both cause hyperactivation of the Hog1p MAP kinase within the high-osmolarity glycerol (HOG) signaling pathway. In the absence of fungicide, Hog1p activation is an essential adaptation enabling fungi to survive conditions of high osmolarity. However, in the presence of these fungicides, this activation of the osmotic signaling pathway leads to cell death. The precise molecular target for these fungicides is yet to be confirmed; however, resistant fungal isolates have been generated in many labs, and many of these resistant strains have mutations in the osmotic-sensing histidine kinase upstream of the MAPK pathway. Under normal conditions, this histidine kinase is active and acts to repress the MAPK pathway. Conditions of high osmolarity or the addition of a fungicide result in the alleviation of the repressive effects of the histidine kinase, and the MAPK pathway is activated. Interestingly, null mutants lacking the histidine kinase are insensitive to fludioxonil but are viable. Quinoxyfen is a protectant fungicide for the prevention of powdery mildew diseases. Following quinoxyfen application, fungal appressorium formation is inhibited, and hyphae are unable to penetrate and infect the host plant. However, once the primary appressorium has formed and the pathogen has infected the plant, quinoxyfen is no longer effective. A strain of Blumeria graminis resistant to quinoxyfen was found to lack a GTPase-activating protein, suggesting that G-protein signaling plays an important role in quinoxyfen sensitivity as well as fungal perception of the host leaf surface and pathogenicity. The molecular target of quinoxyfen and its role in the disruption of fungal signaling is unknown.