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A two‐component signal transduction system involved in nickel sensing in the cyanobacterium Synechocystis sp. PCC 6803
Author(s) -
LópezMaury Luis,
GarcíaDomínguez Mario,
Florencio Francisco J.,
Reyes José C.
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.02741.x
Subject(s) - operon , biology , mutant , synechocystis , gene , promoter , two component regulatory system , transcription (linguistics) , gal operon , l arabinose operon , genetics , response regulator , gene expression , microbiology and biotechnology , linguistics , philosophy
Summary In the cyanobacterium Synechocystis sp. PCC 6803, genes for Ni 2 + , Co 2 + , and Zn 2 + resistance are grouped in a 12 kb gene cluster. The nrsBACD operon is composed of four genes, which encode proteins involved in Ni 2 + resistance. Upstream from nrsBACD , and in opposite orientation, a transcription unit formed by the two genes rppA and rppB has been reported previously to encode a two‐component signal transduction system involved in redox sensing. In this report, we demonstrate that rppA and rppB (here redesigned nrsR and nrsS respectively) control the Ni 2 + ‐dependent induction of the nrsBACD operon and are involved in Ni 2 + sensing. Thus, expression of the nrsBACD operon was not induced by Ni 2 + in a nrsRS mutant strain. Furthermore, nrsRS mutant cells showed reduced tolerance to Ni 2 + . Whereas the nrsBACD operon is transcribed from two different promoters, one constitutive and the other dependent on the presence of Ni 2 + in the medium, the nrsRS operon is transcribed from a single Ni 2 + ‐inducible promoter. The nrsRS promoter is silent in a nrsRS mutant background suggesting that the system is autoregulated. Purified full length NrsR protein is unable to bind to the nrsBACD‐nrsRS intergenic region; however, an amino‐terminal truncated protein that contains the DNA binding domain of NrsR binds specifically to this region. Our nrsRS mutant, which carries a deletion of most of the nrsR gene and part of the nrsS gene, does not show redox imbalance or photosynthetic gene mis‐expression, contrasting with the previously reported nrsR mutant.