Journal
FUNGAL GENETICS AND BIOLOGY
Volume 73, Issue -, Pages 138-149Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.fgb.2014.10.011
Keywords
Conidia; Stress-tolerance; AtfA; Trehalose; MAPK; Aspergillus fumigatus
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Funding
- Noda Institute for Scientific Research
- Japanese Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Related Emerging Mycoses, a Cooperative Research Grant of NEKKEN
- MEXT
- Grants-in-Aid for Scientific Research [25305012] Funding Source: KAKEN
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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 Delta pbsB 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, Delta sa-kA,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. (C) 2014 Elsevier Inc. All rights reserved.
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