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Kenney, L. J.

Publications and source records attributed to Kenney, L. J..

8 recordsLinked to original sources

VopU is a novel T3SS effector protein with mono-ADP-ribosyltransferase activity and a non-canonical H-Y-Q catalytic triad

Vibrio parahaemolyticus utilizes its second Type III Secretion System (T3SS2) to deliver a suite of effector proteins that subvert eukaryotic host cell processes. In this study, we characterize VPA1312, renamed VopU, as a novel T3SS2 effector. We demonstrate that VopU is translocated into infected cells via the T3SS2 and independently of the VocC chaperone. From bioinformatic analyses, VopU is a member of a family of proteins distributed across diverse bacterial taxa and in some cases associated with T6SS gene clusters and plasmids. Sequence, structure-based, and functional analysis reveals that VopU harbors an ADP-ribosyltransferase domain with a non-canonical H-Y-Q catalytic triad, a motif not previously described in naturally occurring mono-ADP-ribosyltransferases. Heterologous expression of VopU within transfected cells or translocation of VopU during infection results in the ADP-ribosylation of a small protein of approximately 18 kDa protein distinct from the target of the previously described ADP-ribosyltransferase effector, VopT. While VopU is not essential for T3SS2-dependent cytotoxicity or intracellular survival of V. parahaemolyticus, heterologous expression of VopU induces host cell rounding and a transcriptional host stress response, likely linked to NAD depletion. These findings provide the initial characterization of this novel family of mono-ADP-ribosyltransferases and expand the known repertoire of bacterial effectors that mediate orthogonal post-translational modifications during host infection. IMPORTANCEVibrio parahaemolyticus is a leading cause of seafood-borne illness worldwide. To cause disease, the bacterium relies on a Type III Secretion System to deliver effector proteins into the cytosol of infected cells, subverting cellular processes. In this study, we identified a novel effector protein, VopU, which performs a post-translational modification known as ADP-ribosylation using a non-canonical catalytic triad (H-Y-Q). This is the first description of a naturally occurring mono-ART with this specific motif. We showed that VopU homologs are distributed across other bacterial species, and that VopU is active during infection of host cells. Together, our findings identify a novel family of effectors that can modify host proteins and potentially contribute to host colonization during infection.

microbiology↗

FLIM Imaging of mCherryTYG Deciphers pH Dynamics and Lifestyles of Salmonella Typhimurium

Intracellular pH regulation is fundamental to bacterial adaptation, virulence, and survival in diverse environments. Salmonella Typhimurium, a key human pathogen, exploits host and environmental pH cues to transition between planktonic, biofilm, and virulence-associated states. However, precise tools to monitor bacterial pH dynamics at subcellular resolution have been limited. Herein, we report the development and application of mCherryTYG, a genetically encoded pH-sensitive fluorophore optimized for fluorescence lifetime imaging (FLIM), enabling robust and high-resolution pH measurements across diverse conditions. mCherryTYG demonstrated exceptional sensitivity across a broad pH range (5.5-8.5) with consistent lifetime responses, and was unaffected by temperature, buffer composition, or ionic strength. Using FLIM, we characterized the pH dynamics of Salmonella across in vitro, host, and biofilm contexts. Under acidic stress in vitro, Salmonella maintained a uniform intracellular pH ([~]6.04), providing clarity on previously debated heterogeneity. In infections of HeLa cells, Salmonella existed in distinct pH environments: acidic vacuolar pH ([~]5.89) and neutral cytoplasmic pH ([~]7.10). During the late infection stage, [~]17% of the bacterial population retained an acidic pH. Biofilm studies revealed stratified pH profiles, with acidic pH near the bottom and neutral pH at the surface, mirroring patterns observed in other pathogens. In heterologous host models, pH gradients shaped bacterial adaptation strategies. In C. elegans, Salmonella experienced a progressive pH gradient from neutral pH ([~]7.10) in the anterior lumen to acidic pH ([~]6.45) in the posterior. Similarly, in zebrafish, Salmonella encountered acidic lysosome-rich enterocytes ([~]5.84) and neutral regions ([~]7.33) in the anterior gut. This study establishes mCherryTYG-FLIM as a transformative tool for studying bacterial pH regulation, revealing pH as a critical modulator of Salmonella lifestyle transitions: virulence, and persistence. Our findings provide new insights into host-microbe interactions and present pH as a promising target for therapeutic interventions against bacterial infections.

microbiology↗

Evaluation of Tumor-colonizing Salmonella Strains using the Chick Chorioallantoic Membrane Model

The chick embryo chorioallantoic membrane (CAM) tumor model is a valuable preclinical model for studying the tumor colonizing process of Salmonella enterica serovar Typhimurium. It offers advantages such as cost-effectiveness, rapid turnaround, reduced engraftment issues, and ease of observation. In this study, we explored and validated the applicability of the partially immune-deficient CAM tumor model. Herein, we demonstrate that Salmonella preferentially colonizes tumors and directly causes tumor cell death. Bacterial migration, tumor colonization, and intra-tumor distribution did not require flagellar-mediated motility. The vast majority of Salmonella that colonized the CAM tumor were extracellular. Thus, tumor invasion was independent of both SPI1- and SPI2-encoded type three secretion systems. Surprisingly, the extracellular residence of Salmonella on CAM tumors did not require biofilm formation. We evaluated our wild-type parental strain compared to the attenuated clinical strain VNP20009 and discovered a reduced tumor colonization capability of VNP20009. The inability to effectively colonize CAM tumors potentially explains the reduced anti-tumor efficacy of VNP20009. Our work establishes the xenograft CAM model as an informative and predictive screening platform for studying tumor-colonizing Salmonella. IMPORTANCECancer has a major impact on society, as it poses a significant health burden to human populations worldwide. Salmonella Typhimurium has demonstrated promise in cancer treatment by exerting direct tumoricidal effects and enhancing host-mediated anti-tumor immunity in xenograft mouse studies. A general understanding of its pathogenesis and the relative ease of genetic manipulation support the development of attenuated strains for therapeutic use. Alternative in ovo models such as the CAM tumor model present a suitable screening platform to accelerate the development of therapeutic strains. It allows for rapid evaluation of Salmonella strains to assess their efficacy and potential as oncolytic agents. The present study establishes that the in ovo tumor model can be utilized as a preclinical tool for evaluating oncolytic Salmonella, bridging the gap between in vitro and in vivo screening.

microbiology↗

RpoS activates Salmonella Typhi biofilms and drives persistence in a Zebrafish model

The development of strategies for targeting the asymptomatic carriage of Salmonella Typhi in chronic typhoid patients has suffered owing to our basic lack of understanding of the molecular mechanisms that enable the formation of S. Typhi biofilms. Traditionally, studies have relied on cholesterol-attached biofilms formed by a closely related serovar, Typhimurium, to mimic multicellular Typhi communities formed on human gallstones. In long-term infections, S. Typhi adopts the biofilm lifestyle to persist in vivo and survive in the carrier state, ultimately leading to the spread of infections via the fecal-oral route of transmission. In the present work, we studied S. Typhi biofilms directly, applied targeted as well as genome-wide genetic approaches to uncover unique biofilm components that do not conform to the CsgD-dependent pathway established in S. Typhimurium. We undertook a genome-wide Tn5 mutation screen in H58, a clinically relevant multidrug resistance strain of S. Typhi, in gallstone-mimicking conditions. We generated New Generation Sequencing libraries based on the ClickSeq technology to identify the key regulators, IraP and RpoS, and the matrix components Sth fimbriae, Vi capsule and lipopolysaccharide. We discovered that the starvation sigma factor, RpoS, was required for the transcriptional activation of matrix-encoding genes in vitro, and for S. Typhi colonization in persistent infections in vivo, using a heterologous fish larval model. An rpoS null mutant failed to colonize the gall bladder in chronic zebrafish infections. Overall, our work uncovered a novel RpoS-driven, CsgD-independent paradigm for the formation of cholesterol-attached Typhi biofilms, and emphasized the role(s) of stress signaling pathways for adaptation in chronic infections. Our identification of the biofilm regulators in S. Typhi paves the way for the development of drugs against typhoid carriage, which will ultimately control the increased incidence of gall bladder cancer in typhoid carriers.

microbiology↗

A pH-sensitive switch activates virulence in Salmonella

The transcriptional regulator SsrB acts as a switch between virulent and biofilm lifestyles of non-typhoidal Salmonella enterica serovar Typhimurium. During infection, phosphorylated SsrB activates genes on Salmonella Pathogenicity Island-2 (SPI-2) essential for survival and replication within the macrophage. Low pH inside the vacuole is a key inducer of expression and SsrB activation. Previous studies demonstrated an increase in SsrB protein levels and DNA-binding affinity at low pH; the molecular basis was unknown (Liew et al., 2019). This study elucidates its underlying mechanism and in vivo significance. Employing single-molecule and transcriptional assays, we report that the SsrB DNA binding domain alone (SsrBc) is insufficient to induce acid pH sensitivity. Instead, His12, a conserved residue in the receiver domain, confers pH sensitivity to SsrB allosterically. Acid-dependent DNA binding was highly cooperative, suggesting a new configuration of SsrB oligomers at SPI-2-dependent promoters. His12 plays a role in SsrB phosphorylation; substituting His12 reduced phosphorylation at neutral pH and abolished pH-dependent differences. Failure to flip the switch in SsrB renders Salmonella avirulent and represents a potential means of controlling virulence.

microbiology↗

Polyimidazolium protects against an invasive clinical isolate of Salmonella Typhimurium

Frequent outbreaks of Salmonella Typhimurium infection in both the animal and human population with potential for zoonotic transmission pose a significant threat to the public health sector. The rapid emergence and spread of more invasive multidrug-resistant clinical isolates of Salmonella further highlight the need for the development of new drugs with effective broad-spectrum bactericidal activities. Synthesis and evaluation of main-chain cationic polyimidazolium 1 (PIM1) against several gram-positive and gram-negative bacteria have previously demonstrated the efficacy profile of PIM1. The present study focuses on antibacterial and anti-biofilm activities of PIM1 against Salmonella both in vitro and in ovo setting. In vitro, PIM1 exhibited bactericidal activity against all tested three strains of Salmonella at a low dosage of 8 g/ml. Anti-biofilm activity of PIM1 was evident with complete inhibition for the initial attachment of biofilms at 16 g/ml and degradation of pre-formed biofilms in a dose-dependent manner. During the host cell infection process, PIM1 reduces extracellular bacterial adhesion and invasion rates to limit the establishment of infection. Once intracellular, the drug-resistant strain was tolerant and protected from PIM1 treatment. In a chicken egg infection model, PIM1 exhibited therapeutic activity for both Salmonella strains with stationary-phase and exponential-phase inocula. Moreover, PIM1 showed a remarkable efficacy against the stationary phase inocula of drug-resistant Salmonella by eliminating the bacteria burden in >50% of infected chicken egg embryos. Collectively, PIM1 has demonstrated its potential as a drug candidate for treatment of Salmonella infections, as well as a solution to tackle egg contamination issues on poultry farms.

microbiology↗

INTS13 Mutations Causing a Developmental Ciliopathy Disrupt Integrator Complex Assembly

Oral-facial-digital syndromes (OFD) are a heterogeneous group of congenital disorders characterized by malformations of the face and oral cavity, and digit anomalies. To date, mutations in 12 ciliary-related genes have been identified that cause several types of OFD, suggesting that OFDs constitute a subgroup of developmental ciliopathies. Through homozygosity mapping and exome sequencing of two families with variable OFD type 2, we identified distinct germline mutations in INTS13, a subunit of the Integrator complex. This 14-component complex associates with RNAPII and can cleave nascent RNA to modulate gene expression. We determined that INTS13 utilizes a discrete domain within its C-terminus to bind the Integrator cleavage module, which is disrupted by the identified germline INTS13 mutations. Depletion of INTS13 disrupts ciliogenesis in human cultured cells and causes dysregulation of a broad collection of ciliary genes. Accordingly, its knockdown in Xenopus embryos lead to motile cilia anomalies. Altogether, we show that mutations in INTS13 cause an autosomal recessive ciliopathy, which reveals key interactions within Integrator components.

biochemistry↗

Formin FHOD1 regulates the size of EPEC pedestals

Enteropathogenic E. coli (EPEC) is an extracellular pathogen that causes polymerization of actin filaments at the site of bacterial attachment, referred to as actin pedestals. Actin polymerization in the pedestal was believed to be solely regulated via the Nck-WASp-Arp2/3 pathway before formins were recently discovered to be associated with pedestals. Herein, we explored the collaborative role of formins in contributing to EPEC pedestal formation. In particular, we discovered that the formin FHOD1 preferentially localized to the pedestal base and its knockdown drastically reduced pedestal surface area. The pedestal localization of formin FHOD1 was found to be dependent on Tir phosphorylation at Y474, and on FHOD1 phosphorylation at Y99 from host Src family kinases (SFKs). Interestingly, differences in Arp2/3 and FHOD1 dynamics were observed. In large pedestals, Arp3 was nearly absent, but FHOD1 levels were high, suggesting that Arp2/3 and formins were segregated temporally. In line with this observation, as the pedestals grew in size, FHOD1 localization increased, while Arp3 localization decreased along the pedestals. Together, our results suggest that EPEC employs multiple actin nucleators that act at different stages of pedestal formation. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=171 SRC="FIGDIR/small/149344v1_ufig1.gif" ALT="Figure 1"> View larger version (43K): org.highwire.dtl.DTLVardef@1711602org.highwire.dtl.DTLVardef@15c060dorg.highwire.dtl.DTLVardef@914447org.highwire.dtl.DTLVardef@119cf28_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗