Functional analyses of 945;-1,3-glucan synthase genes, agsA and agsB, in Aspergillus nidulans

Akira Yoshimi[3] Motoaki sano[1] Tomonori Fujioka[2] Yuko Kokubun[3] Osamu Mizutani[4] Daisuke Hagiwara[3] Takashi Fujikawa[5] Marie Nishimura[5] Fumihiko Hasegawa[3] Keietsu Abe[3]

Author address: 

1KIT, 2Kumiai Chemical Industry Co., Ltd., 3Tohoku Univ. NICHe, 4NRIB, 5NIAS


The cell wall of filamentous fungi is a complex structure that is essential for the maintenance of cell’s shapes and integrity, for the prevention of cell lysis, and for protection against adverse environmental conditions. We previously reported that the transcriptional regulation of a MAP kinase gene mpkA and of cell wall-related genes (CWGs) in Aspergillus nidulans differs significantly from that in Saccharomyces cerevisiae. The transcription of two α -1,3-glucan syntase genes, agsA and agsB, were regulated by MpkA pathway, but most CWGs were not. Recently, the importance of α -1,3-glucan in host-parasite interactions has been studied in both mammalian and plant pathogenic fungi. In this study, to understand the role of α -1,3-glucan in A. nidulans, functional analyses of the agsA and agsB genes were performed. The deletion mutants of agsA gene did not show any significant phenotypes under normal growth conditions. In contrast, the disruptants of agsB gene could not be obtained, suggesting that AgsB seems to play a crucial role in α -1,3-glucan synthesis of A. nidulans. To assess this issue, we constructed the conditional agsB strain whose agsB expression is conditionally regulated under the control of alcA promoter. The transcription of many CWGs coding for β -1,3-glucan synthase and chitin synthase were induced under agsB repressed conditions. This suggests that the decrease of α -1,3-glucan content was counterbalanced by an increase in other cell wall components. The results of the sensitivities to cell wall stress compounds such as micafungin, CFW and Congo Red and the susceptibility test for cell wall degrading enzymes will be presented.

abstract No: 


Full conference title: 

    • ECFG 10th (2010)