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Transcription regulation of the colicin K cka gene reveals induction of colicin synthesis by differential responses to environmental signals.

ABSTRACT: Colicin-producing strains occur frequently in natural populations of Escherichia coli, and colicinogenicity seems to provide a competitive advantage in the natural habitat. A cka-lacZ fusion was used to study the regulation of expression of the colicin K structural gene. Expression is growth phase dependent, with high activity in the late stationary phase. Nutrient depletion induces the expression of cka due to an increase in ppGpp. Temperature is a strong signal for cka expression, since only basal-level activity was detected at 22 degrees C. Mitomycin C induction demonstrates that cka expression is regulated to a lesser extent by the SOS response independently of ppGpp. Increased osmolarity induces a partial increase, while the global regulator integration host factor inhibits expression in the late stationary phase. Induction of cka was demonstrated to be independent of the cyclic AMP-Crp complex, carbon source, RpoS, Lrp, H-NS, pH, and short-chain fatty acids. In contrast to colicin E1, cka expression is independent of catabolite repression and is partially affected by anaerobiosis only upon SOS induction. These results indicate that while different colicins are expressed in response to some common signals such as nutrient depletion, the expression of individual colicins could be further influenced by specific environmental cues.

SUBMITTER: Kuhar I

PROVIDER: S-EPMC103702 | biostudies-literature | 1999 Dec

REPOSITORIES: biostudies-literature

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Transcription regulation of the colicin K cka gene reveals induction of colicin synthesis by differential responses to environmental signals.

Kuhar I I Zgur-Bertok D D

Journal of bacteriology 19991201 23

Colicin-producing strains occur frequently in natural populations of Escherichia coli, and colicinogenicity seems to provide a competitive advantage in the natural habitat. A cka-lacZ fusion was used to study the regulation of expression of the colicin K structural gene. Expression is growth phase dependent, with high activity in the late stationary phase. Nutrient depletion induces the expression of cka due to an increase in ppGpp. Temperature is a strong signal for cka expression, since only b ...[more]

PMID: 10572143

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Project description:BackgroundIt is well established that both cerebral hypoperfusion/stroke and type 2 diabetes are risk factors for Alzheimer's disease (AD). Recently, the molecular link between ischemia/hypoxia and amyloid precursor protein (APP) processing has begun to be established. However, the role of the key common denominator, namely nitric oxide (NO), in AD is largely unknown. In this study, we investigated redox regulation of BACE1, the rate-limiting enzyme responsible for the ?-cleavage of APP to A? peptides.ResultsHerein, we studied events such as S-nitrosylation, a covalent modification of cysteine residues by NO, and H2O2-mediated oxidation. We found that NO and H2O2 differentially modulate BACE1 expression and enzymatic activity: NO at low concentrations (<100 nM) suppresses BACE1 transcription as well as its enzymatic activity while at higher levels (0.1-100 ?M) NO induces S-nitrosylation of BACE1 which inactivates the enzyme without altering its expression. Moreover, the suppressive effect on BACE1 transcription is mediated by the NO/cGMP-PKG signaling, likely through activated PGC-1?. H2O2 (1-10 ?M) induces BACE1 expression via transcriptional activation, resulting in increased enzymatic activity. The differential effects of NO and H2O2 on BACE1 expression and activity are also reflected in their opposing effects on A? generation in cultured neurons in a dose-dependent manner. Furthermore, we found that BACE1 is highly S-nitrosylated in normal aging brains while S-nitrosylation is markedly reduced in AD brains.ConclusionThis study demonstrates for the first time that BACE1 is highly modified by NO via multiple mechanisms: low and high levels of NO suppress BACE1 via transcriptional and post translational regulation, in contrast with the upregulation of BACE1 by H2O2-mediated oxidation. These novel NO-mediated regulatory mechanisms likely protect BACE1 from being further oxidized by excessive oxidative stress, as from H2O2 and peroxynitrite which are known to upregulate BACE1 and activate the enzyme, resulting in excessive cleavage of APP and A? generation; they likely represent the crucial house-keeping mechanism for BACE1 expression/activation under physiological conditions.

Dataset Information

Transcription regulation of the colicin K cka gene reveals induction of colicin synthesis by differential responses to environmental signals.

Publications

Transcription regulation of the colicin K cka gene reveals induction of colicin synthesis by differential responses to environmental signals.

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