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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.