| Literature DB >> 30796472 |
Emi Kunitake1,2, Yi Li1, Ryota Uchida1, Takehiro Nohara1, Keisuke Asano1, Asato Hattori1, Tetsuya Kimura2, Kyoko Kanamaru1, Makoto Kimura1, Tetsuo Kobayashi3.
Abstract
Cellulase production in filamentous fungi is repressed by various carbon sources. In our preliminary survey in Aspergillus nidulans, degree of de-repression differed depending on carbon sources in a mutant of creA, encoding the transcriptional repressor for carbon catabolite repression (CCR). To further understand mechanisms of CCR of cellulase production, we compared the effects of creA deletion with deletion of protein kinase A (pkaA) and G (ganB) genes, which constitute a nutrient sensing and signaling pathway. In plate culture with carboxymethyl cellulose and D-glucose, deletion of pkaA and ganB, but not creA, led to significant de-repression of cellulase production. In submerged culture with cellobiose and D-glucose or 2-deoxyglucose, both creA or pkaA single deletion led to partial de-repression of cellulase genes with the highest level by their double deletion, while ganB deletion caused de-repression comparable to that of the creA/pkaA double deletion. With ball-milled cellulose and D-glucose, partial de-repression was detected by deletion of creA but not of pkaA or ganB. The creA/pkaA or creA/ganB double deletion led to earlier expression than the creA deletion. Furthermore, the effect of each deletion with D-xylose or L-arabinose as the repressing carbon source was significantly different from that with D-glucose, D-fructose, and D-mannose. Consequently, this study revealed that PkaA and GanB participate in CreA-independent CCR and that contribution of CreA, PkaA, and GanB in CCR differs depending on the inducers, repressing carbon sources, and culture conditions (plate or submerged). Further study of CreA-independent mechanisms is needed to fully understand CCR in filamentous fungi.Entities:
Keywords: Aspergillus nidulans; Carbon catabolite repression; Cellulase; GanB; PkaA
Mesh:
Substances:
Year: 2019 PMID: 30796472 DOI: 10.1007/s00294-019-00944-4
Source DB: PubMed Journal: Curr Genet ISSN: 0172-8083 Impact factor: 3.886