In filamentous fungi, group III hybrid histidine kinases (HHKs) are major and nonredundant sensing proteins of the high osmolarity glycerol pathway. In this study, we have compared the biological functions of the two homologous group III HHKs TcsC of Aspergillus fumigatus and NikA of A. nidulans. As expected from previous studies, the corresponding mutants are severely impaired in their ability to adapt to hyperosmotic stress and are both resistant to the antifungal agent fludioxonil. However, our data also reveal novel phenotypes and differences between these mutants. Both TcsC and NikA are required for wild-type-like growth on Czapek-Dox medium and a normal resistance to certain oxidative stressors, whereas an increased resistance to the cell wall disturbing agents Congo red and Calcofluor white was found for the ΔtcsC but not for the ΔnikA mutant. With respect to the cell wall reorganizations that are triggered by fludioxonil in a TcsC/NikA-dependent manner, we observed similarities but also striking differences. Strains from seven Aspergillus species, including A. fumigatus and A. nidulans incorporated more chitin into their cell walls in response to fludioxonil. In contrast, fludioxonil treatment resulted in a shedding of surface accessible galactomannan and β-1,3-glucan in all Aspergillus strains tested except A. nidulans. Hence, the fludioxonil-induced activation of NikA results in a distinct and apparently A. nidulans-specific pattern of cell wall reorganizations that is not due to NikA itself, but its integration into the A. nidulans signaling network.
Keywords: Aspergillus; HOG pathway; fludioxonil; group III HHK.
© The Author(s) 2019. Published by Oxford University Press on behalf of The International Society for Human and Animal Mycology.