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Cell division genes ftsQAZ in Escherichia coli require distant cis ‐acting signals upstream of ddlB for full expression
Author(s) -
Flärdh Klas,
Palacios Pilar,
Vicente Miguel
Publication year - 1998
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.1365-2958.1998.01064.x
Subject(s) - ftsz , biology , lac operon , cell division , transcription (linguistics) , gene , promoter , fusion gene , genetics , reporter gene , escherichia coli , microbiology and biotechnology , gene expression , cell , linguistics , philosophy
A transcriptional reporter fusion has been introduced into the chromosomal ftsZ locus in such a way that all transcription that normally reaches ftsZ can be monitored. The new Φ( ftsZ–lacZ ) fusion yields four times more β‐galactosidase activity than a ddlB–ftsQAZ–lacZ fusion on a lambda prophage vector. A strongly polar ddlB :: Ω insertion prevents contributions from signals upstream of the ftsQAZ promoters and decreases transcription of the chromosomal Φ( ftsZ–lacZ ) fusion by 66%, demonstrating that around two‐thirds of total ftsZ transcription require cis ‐acting elements upstream of ddlB . We suggest that those elements are distant promoters, and thus that the cell division and cell wall synthesis genes in the dcw gene cluster are to a large extent co‐transcribed. The ddlB :: Ω insertion is lethal unless additional copies of ftsQA are provided or a compensatory decrease in FtsZ synthesis is made. This shows that ddlB is a dispensable gene, and reinforces the critical role of the FtsA/FtsZ ratio in septation. Using the new reporter fusion, it is demonstrated that ftsZ expression is not autoregulated.