Borrelia burgdorferi ftsZ Plays a Role in Cell Division.
- From: overman74@xxxxxxxxxxx
- Date: 23 Feb 2006 14:50:37 -0800
J Bacteriol. 2006 Mar;188(5):1969-78.
Borrelia burgdorferi ftsZ Plays a Role in Cell Division.
Dubytska L, Godfrey HP, Cabello FC.
Department of Microbiology and Immunology, New York Medical
College,
Valhalla, NY 10595. .
ftsZ is essential for cell division in many microorganisms. In
Escherichia coli and Bacillus subtilis, FtsZ plays a role in ring
formation at the leading edge of the cell division septum. An ftsZ
homologue is present in the Borrelia burgdorferi genome (ftsZ(Bbu)).
Its
gene product (FtsZ(Bbu)) is strongly homologous to other bacterial FtsZ
proteins, but its function has not been established. Because
loss-of-function mutants of ftsZ(Bbu) might be lethal, the tetR/tetO
system was adapted for regulated control of this gene in B.
burgdorferi.
Sixty-two nucleotides of an ftsZ(Bbu) antisense DNA sequence under the
control of a tetracycline-responsive modified hybrid borrelial promoter
were cloned into pKFSS1. This construct was electroporated into a B.
burgdorferi host strain carrying a chromosomally located tetR under the
control of the B. burgdorferi flaB promoter. After induction by
anhydrotetracycline, expression of antisense ftsZ RNA resulted in
generation of filamentous B. burgdorferi that were unable to divide and
grew more slowly than uninduced cells. To determine whether FtsZ(Bbu)
could interfere with the function of E. coli FtsZ, ftsZ(Bbu) was
amplified from chromosomal DNA and placed under the control of the
tetracycline-regulated hybrid promoter. After introduction of the
construct into E. coli and induction with anhydrotetracycline,
overexpression of ftsZ(Bbu) generated a filamentous phenotype. This
suggested interference of ftsZ(Bbu) with E. coli FtsZ function and
confirmed the role of ftsZ(Bbu) in cell division. This is the first
report of the generation of a B. burgdorferi conditional lethal mutant
equivalent by tetracycline-controlled expression of antisense RNA.
PMID: 16484209 [PubMed - in process]
.
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