Originally published as Genetics Published Articles Ahead of Print on March 4, 2007.

Genetics, Vol. 176, 139-150, May 2007, Copyright © 2007
doi:10.1534/genetics.107.070904

Transcriptional Control of Gluconeogenesis in Aspergillus nidulans

Michael J. Hynes*,1, Edyta Szewczyk*,2, Sandra L. Murray*, Yumi Suzuki*, Meryl A. Davis* and Heather M. Sealy-Lewis{dagger}

* Department of Genetics, University of Melbourne, Victoria, 3010 Australia and {dagger} Department of Biological Sciences, University of Hull, Hull HU6 7RX, England

1 Corresponding author: Department of Genetics, University of Melbourne, Victoria, 3010 Australia.
E-mail: mjhynes{at}unimelb.edu.au

Aspergillus nidulans can utilize carbon sources that result in the production of TCA cycle intermediates, thereby requiring gluconeogenesis. We have cloned the acuG gene encoding fructose-1,6 bisphosphatase and found that expression of this gene is regulated by carbon catabolite repression as well as by induction by a TCA cycle intermediate similar to the induction of the previously studied acuF gene encoding phosphoenolpyruvate carboxykinase. The acuN356 mutation results in loss of growth on gluconeogenic carbon sources. Cloning of acuN has shown that it encodes enolase, an enzyme involved in both glycolysis and gluconeogenesis. The acuN356 mutation is a translocation with a breakpoint in the 5' untranslated region resulting in loss of expression in response to gluconeogenic but not glycolytic carbon sources. Mutations in the acuK and acuM genes affect growth on carbon sources requiring gluconeogenesis and result in loss of induction of the acuF, acuN, and acuG genes by sources of TCA cycle intermediates. Isolation and sequencing of these genes has shown that they encode proteins with similar but distinct Zn(2) Cys(6) DNA-binding domains, suggesting a direct role in transcriptional control of gluconeogenic genes. These genes are conserved in other filamentous ascomycetes, indicating their significance for the regulation of carbon source utilization.