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Lethality of MalE-LacZ hybrid protein shares mechanistic attributes with oxidative component of antibiotic lethality

ABSTRACT: This study examines stress responses following lethal induction of a MalE-LacZ hybrid protein

ORGANISM(S): Escherichia coli str. K-12 substr. MC4100 Escherichia coli

PROVIDER: GSE98505 | GEO | 2017/07/28

SECONDARY ACCESSION(S): PRJNA385309

REPOSITORIES: GEO

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Lethality of MalE-LacZ hybrid protein shares mechanistic attributes with oxidative component of antibiotic lethality.

Project description:Downstream metabolic events can contribute to the lethality of drugs or agents that interact with a primary cellular target. In bacteria, the production of reactive oxygen species (ROS) has been associated with the lethal effects of a variety of stresses including bactericidal antibiotics, but the relative contribution of this oxidative component to cell death depends on a variety of factors. Experimental evidence has suggested that unresolvable DNA problems caused by incorporation of oxidized nucleotides into nascent DNA followed by incomplete base excision repair contribute to the ROS-dependent component of antibiotic lethality. Expression of the chimeric periplasmic-cytoplasmic MalE-LacZ72-47 protein is an historically important lethal stress originally identified during seminal genetic experiments that defined the SecY-dependent protein translocation system. Multiple, independent lines of evidence presented here indicate that the predominant mechanism for MalE-LacZ lethality shares attributes with the ROS-dependent component of antibiotic lethality. MalE-LacZ lethality requires molecular oxygen, and its expression induces ROS production. The increased susceptibility of mutants sensitive to oxidative stress to MalE-LacZ lethality indicates that ROS contribute causally to cell death rather than simply being produced by dying cells. Observations that support the proposed mechanism of cell death include MalE-LacZ expression being bacteriostatic rather than bactericidal in cells that overexpress MutT, a nucleotide sanitizer that hydrolyzes 8-oxo-dGTP to the monophosphate, or that lack MutM and MutY, DNA glycosylases that process base pairs involving 8-oxo-dGTP. Our studies suggest stress-induced physiological changes that favor this mode of ROS-dependent death.

| S-EPMC5576823 | biostudies-literature

Transcription profiling of spinal cord from Math1-LacZ/+ and Math1-LacZ/- E12.5 mice

Project description:C57B6J mice carrying a LacZ allele at the Math1 locus (Math1-LacZ/+) were backcrossed at least 10 generations. The LacZ allele phenocopies a null allele. A total of 5 heterozygous and 5 homozygous null spinal cords were collected (staged at embryonic day 12.5) and individually processed (i.e. not pooled). RNA was extracted and prepared for hybridization to Affymetrix MOE430v2.0 chips under standard conditions (www.affymetrix.com)

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Expression data of Langerhans cells purified from Il34+/LacZ and Il34LacZ/LacZ mice after UV treatment

Project description:We examined the impact of IL-34 on repopulation of Langerhans cells after inflammation Langerhans cells were FACS-purified from Il34+/LacZ and Il34LacZ/LacZ mice after UV treatment

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Addition of RND1 peptide to E. coli BW25113 DELserB, his operator to lacZ transcription fusion.

Project description:Addition of RND1 peptide to E. coli BW25113 (DELserB, his operator to lacZ transcription fusion.

2022-03-31 | PXD014049 | Pride

Hela and LacZ Run Data, plus blanks

Project description:Run containing two samples (Hela and Hela+LacZ), plus blanks

2021-06-18 | MSV000087656 | MassIVE

Gene expression analysis of dissociated and FDG FACS-sorted mammary glands of 16 week old nulliparous AXL +/LacZ and AXL LacZ/LacZ mice (B6.129P2-AXLtm1Dgen strain, Jackson Labs)

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Overexpression of SChLAP1 versus LACZ in RWPE cells

2013-07-20 | GSE40385 | GEO

HEK293 GFP-LacZ-E2F-RFP

Project description:Sequence of transgenic insert incorporating reporter genes GFP-LacZ-E2F-RFP within HEK293 cells

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Overexpression of SChLAP1 versus LACZ in RWPE cells

Project description:SChLAP1 is a novel long non-coding RNA expressed in prostate cancer. Here we performed transcriptional profiling of the benign immortalized prostate cell line RWPE overexpressing two isoforms of the SChLAP-1 lncRNA compared with RWPE overexpressing LACZ. Our goal was to determine the effect of SChLAP1 overexpression on gene expression in prostate cells. Two-condition experiment: RWPE overexpressing SChLAP1 versus RWPE overexpressing LACZ. Biological replicates: 1 control replicate, 2 experimental replicates. Technical replicates: 2 replicates per SChLAP1 isoform. Cell lines: RWPE.

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Comparison of two A. nidulans strains: control CV125 and transgenic NA1363 harboring E. coli LacZ transgene.

Project description:Transcriptional profiling of two A. nidulans strains, aiming to compare the control strain CV125 (pabaA1) with the transgenic strain NA1363 (pabaA1) harbouring a gpdAp-lacZ-trpCt.riboB construct integrated in chromosome VIII. This construct, carried out in a derivative of the pBR322 vector, contained the E. coli lacZ sequence (encoding ß-galactosidase) fused to the A. nidulans trpC terminator and placed under the control of the strong and constitutive promoter of the A. nidulans gpdA gene, and the riboB gene as a selection marker.

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