Search

Questionnaire. It shows items of the self-reporting questionnaire we used in this study. (PDF 83 kb)

Additional file 1:Table S1. PCR primers used in this study. Figure S1. Expression of the genes of the cluster for ustiloxin B biosynthesis in A. oryzae wild-type (RIB40) and ustR EX (G101 and G301) strains grown for 1 day. Figure S2. Expression of the genes of the cluster for ustiloxin B biosynthesis in A. oryzae wild-type (RIB40) and ustR EX (G101 and G301) strains grown for 3 day. Figure S3. Expression of the genes of the cluster for ustiloxin B biosynthesis in A. oryzae wild-type (RIB40) and ustR EX (G101 and G301) strains grown for 7 day. Figure S4. Expression of the genes of the cluster for ustiloxin B biosynthesis in the A. oryzae strains ∆kexB, ustR EX/∆kexB, NSlD-∆P10 (∆P10), and ustR EX/∆P10.

The transcriptional regulation of the MAPK mpkA and cell wall-related genes in Aspergillus nidulans differs from that of their counterparts in Saccharomyces cerevisiae. The A. nidulans MAPK MpkB is putatively orthologous to the yeast MAPKs Kss1p and Fus3p. To investigate MpkB and its contribution to cell wall integrity in A. nidulans, we constructed mpkB-disruptant (mpkB∆) strains. We previously showed that mpkA∆ strains exhibited reduced colony growth and increased sensitivity to the β-1,3-glucan synthase inhibitor micafungin. Like mpkA∆ strains, mpkB∆ strains exhibited slight growth retardation and increased sensitivity to micafungin. Although MpkB-dependent signaling modulated the transcription of some cell wall-related genes, the sugar composition of cell wall fractions was similar among wild-type, mpkA∆, and mpkB∆ strains. To elucidate the relationship between MpkA and MpkB pathways, we compared conditional mutants of mpkB with those with mpkA deletion. Sensitivity testing suggested that MpkA and MpkB additively contribute to micafungin activity in A. nidulans.