Rearranging to resist cell death.

Cytoskeleton rearrangements promote formation of a giant structure called a GUVac that stops cells from dying when they become detached from the extracellular matrix.

Shigella sonnei: epidemiology, evolution, pathogenesis, resistance and host interactions.

Shigella sonnei is a major cause of diarrhoea globally and is increasing in prevalence relative to other Shigella because of multiple demographic and environmental influences. This single-serotype species has traditionally received less attention in comparison to Shigella flexneri and Shigella dysenteriae, which were more common in low-income countries and more tractable in the laboratory. In recent years, we have learned that Shigella are highly complex and highly susceptible to environmental change, as exemplified by epidemiological trends and increasing relevance of S.

Septins promote macrophage pyroptosis by regulating gasdermin D cleavage and ninjurin-1-mediated plasma membrane rupture.

The septin cytoskeleton is primarily known for roles in cell division and host defense against bacterial infection. Despite recent insights, the full breadth of roles for septins in host defense is poorly understood. In macrophages, Shigella induces pyroptosis, a pro-inflammatory form of cell death dependent upon gasdermin D (GSDMD) pores at the plasma membrane and cell surface protein ninjurin-1 (NINJ1) for membrane rupture.

For pet's sake: Discovering a naturally occurring zebrafish virus.

Zebrafish are often used to model host-pathogen interactions, but few models of natural virus infection have been established. A new study in PLOS Biology shows that metatranscriptomics and cohousing experiments can uncover a natural pathogenic virus of zebrafish for laboratory study.

Transcriptional profiling of zebrafish identifies host factors controlling susceptibility to Shigella flexneri.

Shigella flexneri is a human-adapted pathovar of Escherichia coli that can invade the intestinal epithelium, causing inflammation and bacillary dysentery. Although an important human pathogen, the host response to S. flexneri has not been fully described.

induces epigenetic reprogramming of zebrafish neutrophils.

Trained immunity is a long-term memory of innate immune cells, generating an improved response upon reinfection. is an important human pathogen and inflammatory paradigm for which there is no effective vaccine. Using zebrafish larvae, we demonstrate that after training, neutrophils are more efficient at bacterial clearance.

Shigella Serotypes Associated With Carriage in Humans Establish Persistent Infection in Zebrafish.

Shigella represents a paraphyletic group of enteroinvasive Escherichia coli. More than 40 Shigella serotypes have been reported. However, most cases within the men who have sex with men (MSM) community are attributed to 3 serotypes: Shigella sonnei unique serotype and Shigella flexneri 2a and 3a serotypes.

Interplay between septins and ubiquitin-mediated xenophagy during entrapment.

Septins are cytoskeletal proteins implicated in numerous cellular processes including cytokinesis and morphogenesis. In the case of infection by , septins assemble into cage-like structures that entrap cytosolic bacteria targeted by autophagy. The interplay between septin cage entrapment and bacterial autophagy is poorly understood.

An automated microscopy workflow to study Shigella-neutrophil interactions and antibiotic efficacy in vivo.

Shigella are Gram-negative bacterial pathogens responsible for bacillary dysentery (also called shigellosis). The absence of a licensed vaccine and widespread emergence of antibiotic resistance has led the World Health Organisation (WHO) to highlight Shigella as a priority pathogen requiring urgent attention. Several infection models have been useful to explore the Shigella infection process; yet, we still lack information regarding events taking place in vivo.

Septins and K63 ubiquitin chains are present in separate bacterial microdomains during autophagy of entrapped Shigella.

During host cell invasion, Shigella escapes to the cytosol and polymerizes actin for cell-to-cell spread. To restrict cell-to-cell spread, host cells employ cell-autonomous immune responses including antibacterial autophagy and septin cage entrapment. How septins interact with the autophagy process to target Shigella for destruction is poorly understood.

The septin cytoskeleton: Heteromer composition defines filament function.

Septins are an evolutionarily conserved protein family whose members form hetero-oligomeric complexes that assemble into filaments and higher-order structures. In this issue, Martins et al. (2022.

P1 Bacteriophage-Enabled Delivery of CRISPR-Cas9 Antimicrobial Activity Against .

The discovery of clustered, regularly interspaced, short palindromic repeats (CRISPR) and the Cas9 RNA-guided nuclease provides unprecedented opportunities to selectively kill specific populations or species of bacteria. However, the use of CRISPR-Cas9 to clear bacterial infections is hampered by the inefficient delivery of 9 genetic constructs into bacterial cells. Here, we use a broad-host-range P1-derived phagemid to deliver the CRISPR-Cas9 chromosomal-targeting system into and the dysentery-causing to achieve DNA sequence-specific killing of targeted bacterial cells.

Proximity proteomics identifies septins and PAK2 as decisive regulators of actomyosin-mediated expulsion of von Willebrand factor.

In response to tissue injury, within seconds the ultra-large glycoprotein von Willebrand factor (VWF) is released from endothelial storage organelles (Weibel-Palade bodies) into the lumen of the blood vasculature, where it leads to the recruitment of platelets. The marked size of VWF multimers represents an unprecedented burden on the secretory machinery of endothelial cells (ECs). ECs have evolved mechanisms to overcome this, most notably an actomyosin ring that forms, contracts, and squeezes out its unwieldy cargo.

Louis Pasteur continues to shape the future of microbiology.

Louis Pasteur made seminal discoveries in microbiology, immunology and vaccinology that transformed clinical science and saved millions of lives. Since the 19th century, our ability to study infectious disease has undergone radical changes due to newly emerging technologies and infection models. In this Editorial, I consider Pasteur's impact on our ability to understand and combat infectious disease in the context of two modern-day pandemics: coronavirus disease 2019 (COVID-19) and antimicrobial resistance (AMR).

Septins promote caspase activity and coordinate mitochondrial apoptosis.

Apoptosis is a form of regulated cell death essential for tissue homeostasis and embryonic development. Apoptosis also plays a key role during bacterial infection, yet some intracellular bacterial pathogens (such as Shigella flexneri, whose lipopolysaccharide can block apoptosis) can manipulate cell death programs as an important survival strategy. Septins are a component of the cytoskeleton essential for mitochondrial dynamics and host defense, however, the role of septins in regulated cell death is mostly unknown.