Hagiwara Daisuke, Suzuki Satoshi, Kamei Katsuhiko, Gonoi Tohru, Kawamoto Susumu
Medical Mycology Research Center (MMRC), Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8673, Japan.
National Food Research Institute (NFRI), 2-1-12 Kan-nondai, Tsukuba, Ibaraki 305-8642, Japan.
Fungal Genet Biol. 2014 Dec;73:138-49. doi: 10.1016/j.fgb.2014.10.011. Epub 2014 Oct 22.
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.
烟曲霉是一种危及生命的致病真菌，其分生孢子是曲霉病的感染因子。为了更好地理解分生孢子长期存活的潜在机制，我们对一种bZip转录因子AtfA进行了表征，特别关注分生孢子的应激耐受性。atfA缺失突变体分生孢子对高温和氧化应激表现出显著的敏感性。突变体分生孢子中积累的海藻糖含量降低。转录组分析表明，AtfA在分生孢子形成阶段调控了几个与应激保护相关的基因，如catA、dprA、scf1和conJ。上游的高渗甘油途径也参与了分生孢子应激耐受性的赋予，因为ΔpbsB在分生孢子中表现出应激敏感性且海藻糖减少。然而，缺乏SakA丝裂原活化蛋白激酶（MAPK）的突变体产生正常的分生孢子。我们研究了另一种与SakA相关的MAPK，MpkC，双缺失突变体ΔsakA,mpkC在分生孢子应激耐受性方面存在缺陷。我们得出结论，MpkC能够绕过SakA，并且这两种MAPK在烟曲霉中对AtfA的分生孢子相关功能起冗余调节作用。
