J Bacteriol, March 1998, p. 1053-1062, Vol. 180, No. 5
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
andMolecular Control and Genetics, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702
Received 23 October 1997/Accepted 2 January 1998
Inactivation of transcription factor
54, encoded by
rpoN (glnF), restores high-temperature growth
in Luria-Bertani (LB) medium to strains containing the heat-sensitive
cell division mutation ftsZ84. Mutational defects in three
other genes involved in general nitrogen control (glnD,
glnG, and glnL) also suppress lethal
filamentation. Since addition of glutamine to LB medium fully blocks
suppression by each mutation, the underlying cause of suppression
likely derives from a stringent response to the limitation of
glutamine. This model is supported by several observations. The
glnL mutation requires RelA-directed synthesis of the
nutrient alarmone ppGpp to suppress filamentation. Artificially
elevated levels of ppGpp suppress ftsZ84, as do RNA
polymerase mutations that reproduce global effects of the ppGpp-induced
state. Both the glnF null mutation and an elevated copy
number of the relA gene similarly affect transcription from
the upstream (pQ) promoters of the ftsQAZ operon, and both
of these genetic conditions increase the steady-state level of the
FtsZ84 protein. Physiological suppression of ftsZ84 by a
high salt concentration was also shown to involve RelA. Additionally, we found that the growth of a glnF or glnD
strain on LB medium depends on RelA or supplemental glutamine in the
absence of RelA function. These data expand the roles for ppGpp in the
regulation of glutamine metabolism and the expression of FtsZ during
cell division.
Present address: Laboratory of Biochemical Genetics, National
Institute of Mental Health, Bethesda, MD 20892.
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