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Supportive and inhibitory elements of a putative PrfA‐dependent promoter in Listeria monocytogenes
Author(s) -
Luo Qin,
Herler Michael,
MüllerAltrock Stefanie,
Goebel Werner
Publication year - 2005
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 - 10.1111/j.1365-2958.2005.04417.x
Subject(s) - aroa , promoter , biology , transcription (linguistics) , consensus sequence , gene , rna polymerase , sigma factor , genetics , microbiology and biotechnology , gene expression , rna , peptide sequence , escherichia coli , enterobacteriaceae , linguistics , philosophy
Summary Elements essential for PrfA‐dependent transcription were analysed on two promoters of Listeria monocytogenes , the PrfA‐dependent promoter of the phospholipase gene plcA (P plcA ) and a putative promoter of the aroA gene (P aroA2 ) which contains a similar PrfA‐binding site and a similar −10 box as P plcA but does not function as PrfA‐dependent promoter. We constructed a series of hybrid plcA‐aroA promoters by exchanging corresponding sequence elements of these two ‘promoters’. The results showed that the two critical elements of PrfA‐dependent promoters, the PrfA‐box and the −10 box, can be functionally exchanged as long as the distance in between is maintained to 22 or 23 bp. However, the interspace sequence and the sequence downstream of the −10 box of P aroA2 were strongly inhibitory for PrfA‐dependent transcription. A detailed analysis of these two sequences revealed that the RNA polymerase binding site being part of the actual in vivo and in vitro used aroA promoter (P aroA1 ) and a sequence immediately downstream of the putative −10 site, possibly blocking the formation of the open complex, were responsible for the inhibition of PrfA‐dependent transcription from P aroA2 . Taking into consideration the lessons learned from this study we were able to construct a functional PrfA‐dependent aroA promoter.