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FEBS Lett. 2012 Jul 30;586(16):2417-22. doi: 10.1016/j.febslet.2012.05.057. Epub 2012 Jun 8.

Fungal fludioxonil sensitivity is diminished by a constitutively active form of the group III histidine kinase.

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1
Department of Chemistry and Molecular Biology, University of Gothenburg, Box 462, 40530 Gothenburg, Sweden. kentaro.furukawa@cmb.gu.se

Abstract

The fungicide fludioxonil is used to control plant-pathogenic fungi by causing improper activation of the Hog1-type MAPK. However, the appearance of fludioxonil resistant mutants, mostly caused by mutations in the group III histidine kinases, poses a serious problem. Moreover, such mutations cause also hyperosmotic sensitivity and the underlying mechanism has been elusive for a long time. Using Saccharomyces cerevisiae as an experimental host, we show that those phenotypes are conferred by a constitutively active form of the group III histidine kinase. Our results explain the different reasons for fludioxonil resistance conferred by its deletion and missense mutation.

PMID:
22687241
DOI:
10.1016/j.febslet.2012.05.057
[Indexed for MEDLINE]
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