Metabolism of D-galactose is dispensable for the induction of the beta-galactosidase (bgaD) and lactose permease (lacpA) genes in Aspergillus nidulans

Research output: Letter

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Abstract

In this study, we analyze the expression of the Aspergillus nidulans bgaD-lacpA gene couple (encoding an intracellular beta-galactosidase and a lactose permease) in the presence of D-galactose. This monosaccharide can be catabolized via alternative, independent pathways in this model organism. The inductive capabilities of intermediates of the two alternative routes of D-galactose utilization were addressed in loss-of-function mutants defective in a defined step in one of the two pathways. In a galactokinase (galE9) mutant, the cluster is strongly induced by D-galactose, suggesting that formation of Leloir pathway intermediates is not required. The expression profiles of bgaD and lacpA were similar in wild type, L-arabinitol dehydrogenase (araA1), and hexokinase (hxkA1) negative backgrounds, indicating that intermediates of the oxido-reductive pathway downstream of galactitol are not necessary either. Furthermore, bgaD-lacpA transcription was not induced in any of the tested strains when galactitol was provided as the growth substrate. An hxkA1/galE9 double mutant cannot grow on D-galactose at all, but still produced bgaD and lacpA transcripts upon transfer to D-galactose. We therefore concluded that the physiological inducer of the bgaD-lacpA gene cluster upon growth on D-galactose is the nonmetabolized sugar itself.

Original languageEnglish
Pages (from-to)19-25
Number of pages7
JournalFEMS microbiology letters
Volume359
Issue number1
DOIs
Publication statusPublished - jan. 1 2014

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ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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