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- Title
Regulation of formation of the intracellular β-galactosidase activity of Aspergillus nidulans.
- Authors
Fekete, Erzsébet; Karaffa, Levente; Sándor, Erzsébet; Seiboth, Bernhard; Biró, Sándor; Szentirmai, Attila; Kubicek, Christian P.
- Abstract
The regulation of formation of the single intracellular β-galactosidase activity of Aspergillus nidulans was investigated. β-Galactosidase was not formed during growth on glucose or glycerol, but was rapidly induced during growth on lactose or D-galactose. L-Arabinose, and – with lower efficacy – D-xylose also induced β-galactosidase activity. Addition of glucose to cultures growing on lactose led to a rapid decrease in β-galactosidase activity. In contrast, in cultures growing on D-galactose, addition of glucose decreased the activity of β-galactosidase only slightly. Glucose inhibited the uptake of lactose, but not of D-galactose, and required the carbon catabolite repressor CreA for this. In addition, CreA also repressed the formation of basal levels of β-galactosidase and partially interfered with the induction of β-galactosidase by D-galactose, L-arabinose, and D-xylose. D-Galactose phosphorylation was not necessary for β-galactosidase induction, since induction by D-galactose occurred in an A. nidulans mutant defective in galactose kinase, and by the non-metabolizable D-galactose analogue fucose in the wild-type strain. Interestingly, a mutant in galactose-1-phosphate uridylyl transferase produced β-galactosidase at a low, constitutive level even on glucose and glycerol and was no longer inducible by D-galactose, whereas it was still inducible by L-arabinose. We conclude that biosynthesis of the intracellular β-galactosidase of A. nidulans is regulated by CreA, partially repressed by galactose-1-phosphate uridylyl transferase, and induced by D-galactose and L-arabinose in independent ways.
- Subjects
ASPERGILLUS nidulans; ASPERGILLUS; MONILIACEAE; MONILIALES; GLYCOSIDES; GALACTOSE
- Publication
Archives of Microbiology, 2003, Vol 179, Issue 1, p7
- ISSN
0302-8933
- Publication type
Article
- DOI
10.1007/s00203-002-0491-6