A factor that positively regulates cell division by activating transcription of the major cluster of essential cell division genes of Escherichia coli.

Abstract

Cell division in Escherichia coli requires the products of the ftsQ, ftsA and ftsZ genes. It is not known how the cell regulates the cellular concentrations of these essential elements of the division system. We describe here a factor that activates cell division by specifically increasing transcription from one of the two promoters that lie immediately upstream of the ftsQAZ gene cluster. The trans‐acting factor is the product of the sdiA gene, which was isolated on the basis of its ability to suppress the division inhibitory effect of the MinC/MinD division inhibitor. In addition, the sdiA gene product suppressed the action of other chromosomally encoded division inhibitors, induced minicell formation in wild type cells, and restored division activity to an ftsZ temperature‐sensitive mutant grown under nonpermissive conditions. All of these properties were explained by the ability of the sdiA gene product specifically to increase transcription of the ftsQAZ gene cluster, resulting in an increase in cellular concentration of the FtsZ protein. The sdiA gene product is the first factor thus far identified that specifically regulates expression of this key group of cell division genes.

Analysis of the effect of ppGpp on the ftsQAZ operon in Escherichia coli

“…The doublet RNase E cleavage site responsible for the 'pZ1' RNA species represents only 6%. Other estimates of the relative strength of these promoters, based on studies with transcriptional fusions (Yi et al, 1985;Wang et al, 1991;Flä rdh et al, 1997), found about 60% of the total ftsZ mRNA species started from pZ4-pZ3-pZ2-'pZ1', compared with 92% in our study (Table 4). However, the strength of several of these promoters has been shown to vary considerably with growth rate and with growth phase (Dewar et al, 1989;Aldea et al, 1990;Robin et al, 1990;García-Lara et al, 1996;Flärdh et al, 1997).…”

“…When FtsZ is in moderate excess, polar septa are formed, giving rise to minicells Garrido et al, 1993). Moderate overproduction of FtsZ relieves the division inhibition caused by high levels of the division inhibitor SulA (Lutkenhaus et al, 1986), the division inhibitor MinCD (Bi and Lutkenhaus, 1990;Wang et al, 1991) or the trigger factor (Guthrie and Wickner, 1990), as well as that observed in the absence of the molecular chaperone DnaK (Bukau and Walker, 1989). At high FtsZ concentrations, cell division is completely blocked .…”

Control of cell division in Escherichia coli: regulation of transcription of ftsQA involves both rpoS and SdiA-mediated autoinduction.

“…The ftsQAZ gene cluster is regulated by multiple promoters, with the P, and P2 promoters being upstream of the ftsQA genes (24,25). It has been shown that only the P2 promoter is affected by SdiA overexpression (13). Here we show that transcription from the SdiA-regulated P2 promoter satisfies all three requirements of an autoinduction system, suggesting that an autoinduction mechanism is involved in regulation of these genes.…”

“…The SdiA protein from E. coli has an amino acid sequence similar to that of LuxR and has been proposed to activate transcription of the ftsQAZ gene cluster, which is required for cell division (13). The homology between LuxR and SdiA suggested to us the possibility that SdiA might function by a mechanism similar to that of LuxR.…”

“…The autoinduction mechanism in V. fischeri is mediated through a transcriptional activator protein, LuxR, and LuxI, which produces autoinducer from cytoplasmic components (6). There are at least eight other proteins that show extensive similarity to LuxR: SdiA from Escherichia coli (12,13), LasR and RhlR from Pseudomonas aeruginosa (1,14), the nopaline-and octopine-type TraR proteins from Agrobacterium tumefaciens (4,15), RhiR from Rhizobium leguminosarum (16), ExpR from Erwinia carotovora (5), and PhzR from Pseudomonas aureofaciens (3). The structures of seven autoinducers have been determined: V. fischeri autoinducer, N-(3-oxohexanoyl)-Lhomoserine lactone (9); V. harveyi autoinducer, N-(3-hydroxybutanoyl)-L-homoserine lactone (17); A. tumefaciens autoinducer, N-(3-oxooctanoyl)-L-homoserine lactone (18); P. aeruginosa autoinducer, N-(3-oxododecanoyl)-L-homoserine lactone (19); P. aeruginosa factor 2, N-(3-butyryl)-L-homoserine lactone (20); and two other autoinducers produced by V. fischeri-the luxI-independent compound N-octanoyl-Lhomoserine lactone (AI-2), and N-hexanoyl-L-homoserine lactone (AI-3) which is dependent on luxI for its synthesis (21,22).…”