Related Experiment Video

Updated: Nov 3, 2025

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
10:41

Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance

Published on: January 3, 2012

13.5K

Charged Residues Flanking the Transmembrane Domain of Two Related Toxin-Antitoxin System Toxins Affect Host Response

Andrew Holmes1, Jessie Sadlon1, Keith Weaver1

  • 1Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, SD 57069, USA.

Toxins
|June 2, 2021
PubMed

Insights

This study reveals specific amino acid differences in Enterococcus faecalis toxins that cause varied cellular responses. A linked transporter protein limits the toxicity of the chromosomal toxin.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Type I toxin-antitoxin (TA-1) systems produce small, membrane-localized toxins.
  • Initially, TA-1 toxins were thought to kill cells by forming pores, but this is not the mechanism for many.
  • Enterococcus faecalis has two Fst/Ldr family toxins: FstpAD1 (plasmid-encoded) and FstEF0409 (chromosome-encoded).

Purpose of the Study:

  • To identify amino acid differences between FstpAD1 and FstEF0409 responsible for differential transcriptomic responses in E. faecalis.
  • To investigate the role of a transporter protein linked to the chromosomal TA-1 system in modulating toxin toxicity.

Main Methods:

  • Comparative analysis of FstpAD1 and FstEF0409 amino acid sequences.
  • Transcriptomic analysis of E. faecalis cells overexpressing the toxins.
  • Genetic manipulation to assess the function of the linked transporter protein.

Main Results:

  • Specific amino acid variations between FstpAD1 and FstEF0409 were identified as the cause of differential gene induction.
  • A transporter protein genetically linked to the chromosomal TA-1 system was shown to limit the toxicity of FstEF0409.
  • Overexpression of FstpAD1 and FstEF0409 elicits distinct transcriptomic profiles in E. faecalis.

Conclusions:

  • Amino acid sequence dictates the differential cellular impact of Fst/Ldr toxins in E. faecalis.
  • A chromosomal transporter protein plays a regulatory role in mitigating the toxicity of FstEF0409.
  • The mechanism of action for TA-1 toxins is more diverse than previously assumed, involving specific protein interactions and cellular regulation.
Keywords:
Enterococcus faecalisFst/Ldr family toxin 4small protein toxins 3type I toxin–antitoxin system 2

More Related Videos

Transmembrane Domain Oligomerization Propensity determined by ToxR Assay06:45

Transmembrane Domain Oligomerization Propensity determined by ToxR Assay

Published on: May 26, 2011

15.4K
Applying Fluorescence Resonance Energy Transfer FRET to Examine Effector Translocation Efficiency by Coxiella burnetii during siRNA Silencing10:29

Applying Fluorescence Resonance Energy Transfer FRET to Examine Effector Translocation Efficiency by Coxiella burnetii during siRNA Silencing

Published on: July 6, 2016

10.9K

Related Concept Videos

Receptor-mediated Endocytosis01:20

Receptor-mediated Endocytosis

Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
Clathrin-Mediated Endocytosis of LDL
One well-characterized example of receptor-mediated endocytosis is the...
6.9K
Receptor-mediated Endocytosis01:39

Receptor-mediated Endocytosis

Overview
108.1K
Transduction01:16

Transduction

Among the three main modes of HGT—transformation, conjugation, and transduction—transduction is unique in that it is mediated by bacteriophages, or bacterial viruses.Transduction occurs in two ways. Generalized transduction occurs during the lytic cycle of a bacteriophage infection. In this process, bacteriophages infect bacterial cells, replicate within them, and ultimately cause cell lysis, releasing newly assembled virions. Occasionally, random fragments of the bacterial genome...
424
The Two-State Receptor Model01:29

The Two-State Receptor Model

The two-state receptor model explains a drug's interaction with receptors, such as G protein-coupled receptors and ligand-gated ion channels, to induce or inhibit a biological response. When no natural ligands are present, a receptor exists in an equilibrium of inactive (Ri) and active (Ra) conformations. The inactive form does not produce a response, while the active form generates a basal effect known as constitutive activity.
The binding affinity of a drug determines its interaction with...
2.7K
Toxic Reactions: Overview01:26

Toxic Reactions: Overview

When toxic substances penetrate the human body, they disseminate to various tissues, undergoing metabolic changes. This process yields reactive metabolites that may covalently bind with specific target molecules, resulting in toxicity.
Toxicity falls into two primary categories: local and systemic.
Local toxicity appears at the exposure site, such as protein denaturation caused by caustic substances.
In contrast, systemic toxicity requires the toxic agent's absorption and distribution,...
1.4K
Transcription Attenuation in Prokaryotes02:42

Transcription Attenuation in Prokaryotes

Transcriptional attenuation occurs when RNA transcription is prematurely terminated due to the formation of a terminator mRNA hairpin structure.  Bacteria use these hairpins to regulate the transcription process and control the synthesis of several amino acids including histidine, lysine, threonine, and phenylalanine. Transcription attenuation takes place in the non-coding regions of mRNA.
There are several different mechanisms used to attenuate transcription. In ribosome mediated...
16.6K