The mechanism of action of dicarboximides and phenylpyrroles has been studied in
Neurospora crassa. Both fungicides were found to interfere with the signal transduction pathway composed of the following components: osmotic-sensitive (OS)-1 histidine kinase, histidine phosphotransfer protein (HPT)-1, response regulator protein (RRG)-1, OS-4 mitogen-activated protein kinase (MAPK) kinase kinase, OS-5 MAPK kinase, and OS-2 MAPK. All the components, except HPT-1, were essential for the sensitivity to both fungicides and adaptation to osmotic stress. In contrast, the
hpt-1 deletion mutation was lethal unless OS-2 was inactivated. Fludioxonil, osmotic stress, and heat shock induced OS-2 activation by phosphorylation. OS-2 regulated various genes, such as
gcy-1, which encodes glycerol dehydrogenase;
cat-1, which encodes conidial catalase; and the clock-controlled gene (
ccg)
-1. This implies that the signaling pathway plays an important role not only in the stress response but also in asexual differentiation and circadian output. We found 3 types of dicarboximide-resistant mutations in the
BcOS1 gene of
Botrytis cinerea, of which the I365S mutation was dominant in the fields. A hybridization probe assay was developed to detect these mutations in a single polymerase chain reaction that may be suitable for monitoring the development of resistance to various fungicides.
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