Previous Article | Next Article ![]()
Journal of Bacteriology, April 1999, p. 2185-2191, Vol. 181, No. 7
Département de Pathologie,
Université de Genève, Geneva, Switzerland
Received 28 September 1998/Accepted 24 January 1999
Induction of genes expressed from the arabinose PBAD
promoter is very rapid and maximal at low arabinose concentrations. We describe here two mutations that interfere with the expression of genes
cloned under arabinose control. Both mutations map to the
ydeA promoter and stimulate ydeA transcription;
overexpression of YdeA from a multicopy plasmid confers the same
phenotype. One mutation is a large deletion that creates a more
efficient
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Transcriptional Activation of ydeA,
Which Encodes a Member of the Major Facilitator Superfamily, Interferes
with Arabinose Accumulation and Induction of the
Escherichia coli Arabinose PBAD
Promoter

35 region (ATCACA changed to TTCACA), whereas the other
affects the initiation site (TTTT changed to TGTT). The
ydeA gene is expressed at extremely low levels in
exponentially growing wild-type cells and is not induced by arabinose.
Disruption of ydeA has no detectable effect on cell growth.
Thus, ydeA appears to be nonessential under usual
laboratory growth conditions. The ydeA gene encodes a
membrane protein with 12 putative transmembrane segments. YdeA belongs to the largest family of bacterial secondary active transporters, the
major facilitator superfamily, which includes antibiotic resistance exporters, Lac permease, and the nonessential AraJ protein.
Intracellular accumulation of arabinose is strongly decreased in mutant
strains overexpressing YdeA, suggesting that YdeA facilitates arabinose export. Consistent with this interpretation, very high arabinose concentrations can compensate for the negative effect of
ydeA transcriptional activation. Our studies (i) indicate
that YdeA, when transcriptionally activated, contributes to the control
of the arabinose regulon and (ii) demonstrate a new way to modulate the
kinetics of induction of cloned genes.
*
Corresponding author. Mailing address:
Département de Pathologie, Centre Médical Universitaire, 1 rue Michel-Servet, CH-1211 Geneva 4, Switzerland. Phone:
41-22-70.25.769. Fax: 41-22-70.25.746. E-mail:
Dominique.Belin{at}medecine.unige.ch.
Present address: Département de Médecine Interne, HUG,
CH-1211 Geneva 14, Switzerland.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»