NDLI: Regulation of the α-glucuronidase-encoding gene (aguA) from Aspergillus niger

Content Provider	Springer Nature Link
Author	de Vries, R. van de Vondervoort, P. Hendriks, L. van de Belt, M. Visser, J.
Copyright Year	2002
Abstract	The α-glucuronidase gene aguA from Aspergillus niger was cloned and characterised. Analysis of the promoter region of aguA revealed the presence of four putative binding sites for the major carbon catabolite repressor protein CREA and one putative binding site for the transcriptional activator XLNR. In addition, a sequence motif was detected which differed only in the last nucleotide from the XLNR consensus site. A construct in which part of the aguA coding region was deleted still resulted in production of a stable mRNA upon transformation of A. niger. The putative XLNR binding sites and two of the putative CREA binding sites were mutated individually in this construct and the effects on expression were examined in A. niger transformants. Northern analysis of the transformants revealed that the consensus XLNR site is not actually functional in the aguA promoter, whereas the sequence that diverges from the consensus at a single position is functional. This indicates that XLNR is also able to bind to the sequence GGCTAG, and the XLNR binding site consensus should therefore be changed to GGCTAR. Both CREA sites are functional, indicating that CREA has a strong influence on aguA expression. A detailed expression analysis of aguA in four genetic backgrounds revealed a second regulatory system involved in activation of aguA gene expression. This system responds to the presence of glucuronic and galacturonic acids, and is not dependent on XLNR.
Starting Page	96
Ending Page	102
Page Count	7
File Format	PDF
ISSN	16174615
Journal	Molecular and General Genetics MGG
Volume Number	268
Issue Number	1
e-ISSN	16174623
Language	English
Publisher	Springer-Verlag
Publisher Date	2002-07-24
Publisher Place	Berlin/Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Molecular Biology

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