The role of AtfA and HOG MAPK pathway in stress tolerance in conidia of Aspergillus fumigatus

• We characterized AtfA bZip transcription factor and the HOG pathway in pathogenic fungi Aspergillus fumigatus.
• AtfA was essential for trehalose accumulation and resistance to heat and oxidative stresses in conidia.
• AtfA regulates the conidia-related genes responsible for stress protection.
• In the HOG pathway, SakA and MpkC MAPKs function redundantly for the stress tolerance in conidia.

Aspergillus fumigatus is a life-threatening pathogenic fungus, whose conidium is the infectious agent of aspergillosis. To better understand the mechanism underlying the long-term viability of conidia, we characterized a bZip transcription factor, AtfA, with special reference to stress-tolerance in conidia. The atfA deletion mutant conidia showed significant sensitivity to high temperature and oxidative stress. The trehalose content that accumulated in conidia was reduced in the mutant conidia. Transcriptome analysis revealed that AtfA regulated several stress-protection-related genes such as catA, dprA, scf1, and conJ at the conidiation stage. The upstream high-osmolarity glycerol pathway was also involved in conferring stress tolerance in conidia because ΔpbsB showed stress sensitivity and reduced trehalose in conidia. However, a mutant lacking the SakA mitogen-activated protein kinase (MAPK) produced normal conidia. We investigated another MAPK, MpkC, in relation with SakA, and the double deletion mutant, ΔsakA,mpkC, was defective in conidia stress tolerance. We concluded that MpkC is able to bypass SakA, and the two MAPKs redundantly regulate the conidia-related function of AtfA in A. fumigatus.