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Fungal fludioxonil sensitivity is diminished by a constitutively active form of the group III histidine kinase
Author(s) -
Furukawa Kentaro,
Randhawa Anmoldeep,
Kaur Harsimran,
Mondal Alok K.,
Hohmann Stefan
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.05.057
Subject(s) - fludioxonil , histidine kinase , histidine , saccharomyces cerevisiae , kinase , mutant , missense mutation , biology , mutation , biochemistry , chemistry , yeast , microbiology and biotechnology , fungicide , genetics , enzyme , botany , gene
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.