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RNA-sequencing analysis examining how the Vibrio cholerae MARTX toxin and its inidividual effector domains modulate the transcriptome of human intestinal epithelial cells.

ABSTRACT: RNA-sequencing analysis examining how the Vibrio cholerae MARTX toxin and its inidividual effector domains modulate the transcriptome of human intestinal epithelial cells.

PROVIDER: PRJNA516425 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8472730.fastq.gz	Fastqsanger.gz
	SRR8472721.fastq.gz	Fastqsanger.gz
	SRR8472731.fastq.gz	Fastqsanger.gz
	SRR8472722.fastq.gz	Fastqsanger.gz
	SRR8472732.fastq.gz	Fastqsanger.gz

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RNA-sequencing analysis examining how the Vibrio cholerae MARTX toxin and its inidividual effector domains modulate the transcriptome of human intestinal epithelial cells.

Project description:MARTX toxins are large single polypeptide bacterial toxins that translocate multiple cytotoxic and functionally independent effector domains into the cytosol of a target eukaryotic cell. Pandemic Vibrio cholerae El Tor O1 strains secrete a MARTX toxin with three effector domains — the actin crosslinking domain (ACD), the Rho inactivation domain (RID), and the alpha/beta-hydrolase domain (ABH) — to regulate innate immunity and enhance colonization. The goal of this study was to compare changes in the transcriptome of human intestinal epithelial cells (IECs) treated with V. cholerae modified to secret a toxin with only one effector domain to the transcriptome of cells treated with V. cholerae secreting the wild type MARTX toxin that delivers all three effector domains simultaneously. We demonstrate that when all three effectors are delivered there is no change in transcriptional response of IECs compared to untreated cells. However, when only ACD is delivered, transcriptional profiling revealed a significant proinflammatory response is activated. These data suggests that V. cholerae may utilize co-delivery of RID and/or ABH to silence the intestinal immune response to ACD activity. These data provide insight into how the V. cholerae MARTX toxin effector domains function together to alter the innate immune response of IECs during bacterial infection.

2019-01-23 | GSE125453 | GEO

Vibrio vulnificus MARTX toxin effector domains differentially remodel the transcriptional response of intestinal epithelial cells

Project description:Vibrio vulnificus is an foodborne pathogen that can cause gastroenteritis and septicemia in humans. V. vulnificus secretes a multifunctional autoprocessing repeats-in-toxin (MARTX) toxin as an essential virulence factor to cause disease. MARTX toxins are pore-forming toxins that translocate multiple functionally independent effector domains into a target cell. MARTX toxins of V. vulnificus can contain anywhere from 3 to 5 of the 10 identified effector domains and strains with different effector repertories having varying virulence potential. The goal of this study was to compare how different effector combinations from an F-type MARTX toxin differentially remodel the transcriptional response of human intestinal epithelial cells (IECs). F-type MARTX toxins contain five effector domains – the actin crosslinking domain (ACD), two copies the makes caterpillar floppy-like domain (MCF), and alpha-beta hydrolase (ABH) domain, and the Ras/Rap1 specific endopeptidase (RRSP). Cultured human IECs were treated with V. vulnificus or strains modified to secrete a toxin with only ACD, ACD with MCF-ABH, ACD with RRSP, or no active effectors. We demonstrate that when no active effectors are present, the bacterium induces minimal changes in the transcriptional profile of IECs. However, the strains containing different effector combinations each uniquely remodeled the transcriptional profile of IECs. These data provide insight into how V. vulnificus strains with varying effector combinations can differentially regulate the host cell response to cause disease.

2021-11-21 | GSE189194 | GEO

Vibrio vulnificus MARTX toxin effector domains differentially remodel the transcriptional response of intestinal epithelial cells

Project description:Vibrio vulnificus MARTX toxin effector domains differentially remodel the transcriptional response of intestinal epithelial cells

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Engineering effector domains of MEF2C and GATA4 enhances cardiac reprogramming

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Invasion strategy of pathogenic bacteria is reinforced by a MARTX toxin effector duet

Project description:Multiple bacterial genera take advantage of the multifunctional utoprocessing repeats-in-toxin (MARTX) toxin to invade host cells1. Secretion of the MARTX toxin by Vibrio vulnificus, a deadly opportunistic pathogen that causes primary septicemia, the precursor of sepsis2-5, is a major driver of infection6,7; however, it is not clear how the toxin induces septicemia. Here, we report the crystal and cryo-electron microscopy (EM) structures of a toxin effector duet comprising the domain of unknown function in the first position (DUF1)/Rho inactivation domain (RID) complexed with human targets. These structures reveal how the duet is used by bacteria as a potent weapon. The data show that DUF1 acts as a RID-dependent transforming NADase domain (RDTND) that disrupts NAD+ homeostasis by hijacking calmodulin. The cryo-EM structure of the RDTND-RID duet complexed with calmodulin and Rac1, together with immunological analyses in vitro and in mice, provide mechanistic insight into how V. vulnificus uses the duet to suppress ROS generation by depleting NAD(P)+ and modifying Rac1 in a mutually-reinforcing manner that ultimately paralyzes first line immune responses, promotes dissemination of invaders, and induces sepsis. These data may allow development of tools or strategies to combat MARTX toxin-related human diseases.

2024-07-05 | PXD047927 | Pride

Engineering effector domains of MEF2C and GATA4 enhances cardiac reprogramming

Project description:The transcription factors MEF2C, GATA4, and TBX5 (MGT) are well established for converting fibroblasts into induced cardiomyocytes (iCMs). However, these reprogramming factors contain effector domains, yet their functional roles in cardiac reprogramming remain largely uncharacterized. Furthermore, whether internal deletions of these domains improve or compromise reprogramming efficiency has not been elucidated. Here we found that the combination of MEF2C and GATA4 mutants (MΔGΔT) elevated reprogramming efficiency by 7-fold to ~21%, achieving robust induction of iCMs with well-defined sarcomeric structures.

2025-06-30 | GSE300140 | GEO

The Modes of Action of MARTX Toxin Effector Domains.

Project description:Many Gram-negative bacterial pathogens directly deliver numerous effector proteins from the bacterium to the host cell, thereby altering the target cell physiology. The already well-characterized effector delivery systems are type III, type IV, and type VI secretion systems. Multifunctional autoprocessing repeats-in-toxin (MARTX) toxins are another effector delivery platform employed by some genera of Gram-negative bacteria. These single polypeptide exotoxins possess up to five effector domains in a modular fashion in their central regions. Upon binding to the host cell plasma membrane, MARTX toxins form a pore using amino- and carboxyl-terminal repeat-containing arms and translocate the effector domains into the cells. Consequently, MARTX toxins affect the integrity of the host cells and often induce cell death. Thus, they have been characterized as crucial virulence factors of certain human pathogens. This review covers how each of the MARTX toxin effector domains exhibits cytopathic and/or cytotoxic activities in cells, with their structural features revealed recently. In addition, future directions for the comprehensive understanding of MARTX toxin-mediated pathogenesis are discussed.

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Engineering of effector domains for targeted DNA methylation with reduced off-target effects

Project description:Engineering of effector domains for targeted DNA methylation with reduced off-target effects

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Staphylococcus aureus toxin-antitoxin system

Project description:Type I toxin-antitoxin (TA) systems are widespread genetic modules in bacterial genomes. They express toxic peptides whose overexpression leads to growth arrest or cell death, whereas antitoxins regulate the expression of toxins, acting as labile antisense RNAs. The Staphylococcus aureus (S. aureus) genome contains and expresses several functional type I TA systems, but their biological functions remain unclear. Here we addressed and challenged experimentally, by proteomics, if a type I TA system, the SprF1/SprG1 pair, influences the overall gene expression in S. aureus. Deleted and complemented S. aureus strains were analyzed for their proteomes, both intracellular and extracellular, during growth. Comparison of intracellular proteomes between the strains points on SprF1 antitoxin as an agent downregulating protein expression. In the strain naturally expressing the SprG1 toxin, cytoplasmic proteins are excreted into the medium, but this is not due to unspecific cell leakages. Such toxin-driven release of the cytoplasmic proteins may modulate the host inflammatory response that, in turn, may amplify the S. aureus infection spread.

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