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Enterohemorrhagic Escherichia coli effector EspF triggers oxidative DNA lesions in intestinal epithelial cells

ABSTRACT: Enterohemorrhagic Escherichia coli effector EspF triggers oxidative DNA lesions in intestinal epithelial cells

PROVIDER: PRJNA1073570 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27882222_1.fastq.gz	Fastqsanger.gz
	SRR27882222_2.fastq.gz	Fastqsanger.gz
	SRR27882223_1.fastq.gz	Fastqsanger.gz
	SRR27882223_2.fastq.gz	Fastqsanger.gz
	SRR27882224_1.fastq.gz	Fastqsanger.gz

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Enterohemorrhagic Escherichia coli effector EspF triggers oxidative DNA lesions in intestinal epithelial cells

Project description:Attaching/effacing(A/E) pathogens induce DNA damage and colorectal cancer by injecting effector proteins into host cells via the type III secretion system (T3SS). EspF is one of the T3SS-dependent effector proteins exclusive to A/E pathogens, which include enterohemorrhagicEscherichia coli(EHEC). The role of EspF in the induction of double-strand breaks (DSBs) and the phosphorylation of the repair protein SMC1 has been demonstrated previously. However, the process of damage accumulation and DSB formation has remained enigmatic, and the damage response is not well understood. Here, we first showed a compensatory increase in the mismatch repair (MMR) proteins MutS homolog 2 (MSH2) and MSH6, as well as poly(ADP-ribose) polymerase 1 (PARP1), followed by a dramatic decrease, threatening cell survival in the presence of EspF. Flow cytometry revealed that EspF arrested the cell cycle at the G2/M phase to facilitate DNA repair. Subsequently, 8-oxoguanine (8-oxoG) lesions, a marker of oxidative damage, were assayed by ELISA and immunofluorescence, which revealed the accumulation of 8-oxoG from the cytosol to the nucleus. Furthermore, the status of single-stranded DNA (ssDNA) and DSBs was confirmed. We observed that EspF accelerated the course of DNA lesions, including 8-oxoG and unrepaired ssDNA, which were converted into DSBs; this was accompanied by the phosphorylation of Replication protein A 32 (RPA32) in repair-defective cells. Collectively, these findings reveal that EspF triggers various types of oxidative DNA lesions with impairment of the DNA damage response and may result in genomic instability and cell death, offering novel insight into the tumorigenic potential of EspF.

2024-02-14 | GSE255129 | GEO

Oligodendrocyte degeneration triggers the formation of inflammatory brain lesions

Project description:Oligodendrocyte degeneration triggers the formation of inflammatory brain lesions

| PRJNA489884 | ENA

Tumor-derived oxidative stress triggers follicle loss in breast cancer

Project description:Tumor-derived oxidative stress triggers follicle loss in breast cancer

| PRJNA858670 | ENA

Escherichia coli strain:Enterohemorrhagic

Project description:Escherichia coli strain:Enterohemorrhagic Genome sequencing

| PRJNA723701 | ENA

Oligodendrocyte degeneration triggers the formation of inflammatory brain lesions

Project description:Here, we investigated whether cuprizone-induced oligodendrocyte apoptosis is sufficient to trigger peripheral immune cell recruitment into the forebrain. We show that early cuprizone-induced white matter lesions display a striking similarity to early MS lesions, i.e., oligodendrocyte degeneration, microglia activation and absence of lymphocytes. Such early cuprizone lesions are sufficient to trigger peripheral immune cell recruitment. The lesions are characterized by discontinuation of the perivascular glia limitans, focal axonal damage, and perivascular astrocyte pathology. Time course studies showed that the severity of cuprizone-induced lesions positively correlates with the extent of peripheral immune cell recruitment. Furthermore, results of genome-wide array analyses suggest that moesin is integral for early microglia activation in cuprizone and MS lesions. This study underpins the significance of brain-intrinsic degenerative cascades for immune cell recruitment and, in consequence, MS lesion formation.

2021-09-07 | GSE119672 | GEO

Proteasome inhibition and oxidative biochemistry are synergistic triggers of metabolic heme toxicity

Project description:Proteasome inhibition and oxidative biochemistry are synergistic triggers of metabolic heme toxicity

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The Enterohemorrhagic Escherichia coli Effector EspW Triggers Actin Remodeling in a Rac1-Dependent Manner.

Project description:Enterohemorrhagic Escherichia coli (EHEC) is a diarrheagenic pathogen that colonizes the gut mucosa and induces attaching-and-effacing lesions. EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack and manipulate host cell signaling pathways, which allow bacterial colonization and subversion of immune responses and disease progression. The aim of this study was to characterize the T3SS effector EspW. We found espW in the sequenced O157:H7 and non-O157 EHEC strains as well as in Shigella boydii Furthermore, a truncated version of EspW, containing the first 206 residues, is present in EPEC strains belonging to serotype O55:H7. Screening a collection of clinical EPEC isolates revealed that espW is present in 52% of the tested strains. We report that EspW modulates actin dynamics in a Rac1-dependent manner. Ectopic expression of EspW results in formation of unique membrane protrusions. Infection of Swiss cells with an EHEC espW deletion mutant induces a cell shrinkage phenotype that could be rescued by Rac1 activation via expression of the bacterial guanine nucleotide exchange factor, EspT. Furthermore, using a yeast two-hybrid screen, we identified the motor protein Kif15 as a potential interacting partner of EspW. Kif15 and EspW colocalized in cotransfected cells, while ectopically expressed Kif15 localized to the actin pedestals following EHEC infection. The data suggest that Kif15 recruits EspW to the site of bacterial attachment, which in turn activates Rac1, resulting in modifications of the actin cytoskeleton that are essential to maintain cell shape during infection.

| S-EPMC5563575 | biostudies-literature

FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice

Project description:FAM3C/ILEI protein is elevated in psoriatic lesions and triggers psoriasiform hyperproliferation in mice

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Self-incompatibility triggers irreversible oxidative modification of proteins in incompatible pollen

Project description:Self-incompatibility (SI) is used by many angiosperms to prevent self-fertilization and inbreeding. In Papaver rhoeas interaction of cognate pollen and pistil S-determinants triggers programmed cell death (PCD) of incompatible pollen. We previously identified that reactive oxygen species (ROS) signals to SI-PCD. ROS induced oxidative post-translational modifications (oxPTMs) can regulate protein structure and function. Here we have identified and mapped oxPTMs triggered by SI in incompatible pollen. Notably, SI-induced pollen had numerous irreversible oxidative modifications; untreated pollen had virtually none. Our data provide the first analysis of the protein targets of ROS in the context of SI-induction and represent a milestone because currently there are few reports of irreversible oxPTMs in plants. Strikingly, cytoskeletal proteins and enzymes involved in energy metabolism are a prominent target. Oxidative modifications to a phosphomimic form of a pyrophosphatase result in a reduction of its activity. Therefore, our results demonstrate irreversible oxidation of pollen proteins during SI and show that this can affect protein function. We suggest that this reduction in cellular activity could lead to PCD.

2020-04-02 | MSV000085216 | MassIVE

Enterohemorrhagic Escherichia coli: impact of short chain fatty acid treatment on virulence gene expression

Project description:transcriptome analysis of enterohemorrhagic E. coli treated with either one of two different concentrations of short chain fatty acid mixes or the corresponding sodium chloride osmolarity control

2016-03-23 | GSE79509 | GEO

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