Mechanism of action of dicarboximide and phenylpyrrole on the stress-response signal transduction pathway

• Published in: Journal of Pesticide Science 2010/08/25, Vol.35(3), pp.351-353
• Main Author: Fujimura, Makoto
• Format: Article
• Language: English
• Subjects: histidine kinase; MAP kinase; Neurospora crassa; osmotic stress
• ISSN: 1348-589X; 1349-0923
• DOI: 10.1584/jpestics.J10-02

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.