JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Michel, K.-P.
Right arrow Articles by Golden, S. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Michel, K.-P.
Right arrow Articles by Golden, S. S.

 Previous Article  |  Next Article 

Journal of Bacteriology, September 2001, p. 5015-5024, Vol. 183, No. 17
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.17.5015-5024.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Unusual Regulatory Elements for Iron Deficiency Induction of the idiA Gene of Synechococcus elongatus PCC 7942

Klaus-Peter Michel,1,2 Elfriede K. Pistorius,2 and Susan S. Golden1,*

Department of Biology, Texas A&M University, College Station, Texas 77843-3258,1 and Biologie VIII: Zellphysiologie, Universitaet Bielefeld, D-33615 Bielefeld, Germany2

Received 22 February 2001/Accepted 6 June 2001

Expression of a thylakoid membrane-associated protein called IdiA (iron-deficiency-induced protein A) is highly elevated and tightly regulated by iron limitation in Synechococcus elongatus PCC 6301 and PCC 7942. Although this protein is not essential for photosystem II (PSII) activity, it plays an important role in protecting the acceptor side of PSII against oxidative damage, especially under iron-limiting growth conditions, by an unknown mechanism. We defined the iron-responsive idiA promoter by using insertional inactivation mutagenesis and reporter gene assays. A 67-bp DNA region was sufficient for full iron deficiency-inducible idiA promoter activity. Within this fragment is a palindromic sequence 4 bp upstream of a putative -35 promoter element, which resembles the binding site of FNR/CAP-type helix-turn-helix transcription factors. The absence of this palindromic sequence or a 3-bp mutation in a putative -10 region eliminated promoter activity completely. A previously identified candidate for a positively acting transcription factor is the IdiB protein, whose gene lies immediately downstream of idiA. IdiB shows strong similarity to helix-turn-helix transcription factors of the FNR/CAP family. A His6x-tagged IdiB that was overexpressed in Escherichia coli bound to a 59-bp fragment of the idiA regulatory region that included the palindrome. Although the idiA promoter lacks a consensus binding site for the iron-sensing regulator Fur, we attempted to inactivate fur in order to investigate the potential role of this factor. The resulting merodiploid mutants showed constitutive partial derepression of IdiA expression under iron-sufficient growth conditions. We concluded that IdiB is a specific iron-responsive regulator of idiA and that Fur has an indirect role in influencing idiA expression.

* Corresponding author. Mailing address: Department of Biology, Texas A&M University, College Station, TX 77843-3258. Phone: (979) 845-9824. Fax: (979) 862-7659. E-mail: sgolden{at}tamu.edu.

Journal of Bacteriology, September 2001, p. 5015-5024, Vol. 183, No. 17
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.17.5015-5024.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2001 by the American Society for Microbiology. All rights reserved.