Microreviews, Review

Escherichia coli hijack Caspr1 receptor to invade cerebral vascular and neuronal hosts

Wei-Dong Zhao1, Dong-Xin Liu1, Yu-Hua Chen1

In this article, the authors comment on the study "Caspr1 is a host receptor for meningitis-causing Escherichia coli" by Zhao et al. (Nat Commun, 2ß18) that identified Caspr1 as a key host receptor for E. coli virulence factor IbeA, facilitating E. coli penetration through the blood-brain barrier (BBB). The research demonstrated that targeting the interaction between IbeA and Caspr1 could potentially neutralize E. coli virulence and prevented meningitis, shedding light on the mechanisms of bacterial invasion into brain endothelial cells and hippocampal neurons.

A global view of substrate phosphorylation and dephosphorylation during budding yeast mitotic exit

Sandra A. Touati1 and Frank Uhlmann1

In this article, the authors comment on the study "Phosphoproteome dynamics during mitotic exit in budding yeast" by Touati (EMBO J, 2018) that described a time-resolved global phosphoproteome analysis during a cell cycle phase known as mitotic exit in budding yeast revealed the principles of phosphoregulation governing the ordered sequence of events such as spindle elongation, chromosome decondensation, and completion of cell division.

Gammaretroviruses tether to mitotic chromatin by directly binding nucleosomal histone proteins

Madushi Wanaguru1 and Kate N. Bishop1

In this article, the authors comment on the study "Murine leukemia virus p12 tethers the capsid-containing pre-integration complex to chromatin by binding directly to host nucleosomes in mitosis" by Wanaguruet al. (PLoS Pathog, 2018) that highlights the essential role of the gammaretroviral gag cleavage product, p12, at both early and late stages of the virus life cycle, particularly in the integration of the viral DNA into the host cell chromatin to form a provirus. It also emphasizes the recent findings regarding the N- and C-terminal domains of p12, revealing their direct binding to the viral capsid lattice and nucleosomal histone proteins, respectively, thus elucidating the mechanism by which p12 links the viral pre-integration complex to mitotic chromatin.

Methodologies for in vitro and in vivo evaluation of efficacy of antifungal and antibiofilm agents and surface coatings against fungal biofilms

Patrick Van Dijck1,2,‡, Jelmer Sjollema3,‡, Bruno P.A. Cammue4,5, Katrien Lagrou6,7, Judith Berman8, Christophe d’Enfert9, David R. Andes10,11, Maiken C. Arendrup12-14, Axel A. Brakhage15, Richard Calderone16, Emilia Cantón17, Tom Coenye18,19, Paul Cos20, Leah E. Cowen21, Mira Edgerton22, Ana Espinel-Ingroff23, Scott G. Filler24, Mahmoud Ghannoum25, Neil A.R. Gow26, Hubertus Haas27, Mary Ann Jabra-Rizk28, Elizabeth M. Johnson29, Shawn R. Lockhart30, Jose L. Lopez-Ribot31, Johan Maertens32, Carol A. Munro26, Jeniel E. Nett33, Clarissa J. Nobile34, Michael A. Pfaller35,36, Gordon Ramage19,37, Dominique Sanglard38, Maurizio Sanguinetti39, Isabel Spriet40, Paul E. Verweij41, Adilia Warris42, Joost Wauters43, Michael R. Yeaman44, Sebastian A.J. Zaat45, Karin Thevissen4,*

This article highlights the critical importance of accurate susceptibility testing methods and the discovery of novel antifungal and antibiofilm agents in combating invasive fungal infections associated with biofilm formation on medical devices, thereby emphasizing the need for advancements in medical mycology research to address these complex diseases.

Shepherding DNA ends: Rif1 protects telomeres and chromosome breaks

Gabriele A. Fontana1, Julia K. Reinert1,2, Nicolas H. Thomä1, Ulrich Rass1

This review discusses the conserved mechanisms cells have evolved to protect DNA ends at chromosomal termini and DNA double-strand breaks (DSBs), focusing on the protein Rif1’s roles in telomere homeostasis and DSB repair in eukaryotes. It highlights the intriguing connection between Rif1's involvement in both telomere maintenance and DSB repair, and suggests that excluding end-processing factors may underlie Rif1's diverse biological functions at telomeres and chromosome breaks.

The CRISPR conundrum: evolve and maybe die, or survive and risk stagnation

Jesús García-Martínez1, Rafael D. Maldonado1, Noemí M. Guzmán1 and Francisco J. M. Mojica1,2

In this article García-Martínez et al. cover how the model bacterium Escherichia coli deals with CRISPR-Cas to tackle the major dilemma of evolution versus survival.

A novel mechanism for regulation of the type I IFN response by herpesvirus deconjugases

Soham Gupta1, Päivi Ylä-Anttila1, Maria G. Masucci1

In this article, the authors comment on the study "Herpesvirus deconjugases inhibit the IFN response by promoting TRIM25 autoubiquitination and functional inactivation of the RIG-I signalosome" by Gupta et al. (PLoS Pathog, 2018), discussing the finding of a novel mechanism for regulation of the type I IFN response by herpesvirus deconjugases.

Metabolic disharmony and sibling conflict mediated by T6SS

Vera Troselj1 and Daniel Wall1

In this article, the authors comment on the study "Physiological Heterogeneity Triggers Sibling Conflict Mediated by the Type VI Secretion System in an Aggregative Multicellular Bacterium" by Troselj et al. (MBio, 2018) discussing that M. xanthus uses T6SS to eliminate less fit cells from their population and identified toxic effector and cognate immunity protein (TsxEI) that mediates this sibling antagonism.

Helicobacter hepaticus polysaccharide induces an anti-inflammatory response in intestinal macrophages

Camille Danne1 and Fiona Powrie1

In this article, the authors comment on the study "A Large Polysaccharide Produced by Helicobacter hepaticus Induces an Anti-inflammatory Gene Signature in Macrophages. " by Danne et al, (Cell Host Microbe 2017), discussing the interactions between H. hepaticus and intestinal macrophages that promote mutualism.

Previous Next

Post-transcriptional regulation of ribosome biogenesis in yeast

May 1, 2017

Microorganisms adapt to environmental changes by regulating their metabolism, and one key survival strategy is to decrease energy use during adverse conditions by halting ribosome production, with recent findings showing yeast can switch between pre-rRNA processing pathways in response to environmental shifts, adding complexity to ribosome biogenesis regulation.

Insights from the redefinition of Helicobacter pylori lipopolysaccharide O-antigen and core-oligosaccharide domains

April 25, 2017

This article comments on work published by Li et al. (PloS Pathog, 2017), focusing on Helicobacter pylori infections. They are mostly asymptomatic but can lead to serious conditions, and H. pylori lipopolysaccharide (LPS) is crucial for colonization and persistence, making the study of its structure and biosynthesis pathway vital for understanding pathogenesis and developing treatments.

Evading plant immunity: feedback control of the T3SS in Pseudomonas syringae

March 17, 2017

This article comments on work published by Waite et al. (mBio, 2017), which indicates that a negative autogenous control mechanism, where the sigma factor HrpL represses its own expression, permits the plant pathogen Pseudomonas syringae to fine-tune its type III secretion system, potentially reducing the elicitation of plant immunity and enhancing its ability to cause disease.

Microbial flora, probiotics, Bacillus subtilis and the search for a long and healthy human longevity

March 16, 2017

This article comments on work published by Donato et al. (Nat Commun, 2017), which reveals that the probiotic Bacillus subtilis extends the lifespan of Caenorhabditis elegans via mechanisms including the formation of biofilms and the production of signaling molecules like NO and CSF, suggesting a potential pathway through insulin-like signaling that could impact human longevity and age-related diseases.

Chlamydia trachomatis’ struggle to keep its host alive

March 2, 2017

This article comments on work published by Sixt et al. (Cell Host Microbe, 2016), which analyzed a CpoS-deficient mutant yielding unique insights into the nature of cell-autonomous defense responses against Chlamydia.

New insights into the function of a versatile class of membrane molecular motors from studies of Myxococcus xanthus surface (gliding) motility

March 2, 2017

This article comments on work published by Faure et al. (Nature, 2016), which deciphers force transmission at focal adhesion complexes that are involved in gliding motility in bacteria.

Advancing host-directed therapy for tuberculosis: new therapeutic insights from the Toxoplasma gondii

March 2, 2017

This article comments on work published by Koh et al. (PLoS Pathog, 2017), which uncovered that infection-induced signaling pathways suggest possibilities for the development of novel therapeutic modalities for TB that target the intracellular signaling pathways permitting the replication of Mycobacterium tuberculosis (MTB).

Breaking the bilayer: OMV formation during environmental transitions

February 3, 2017

This article comments on work published by Bonnington & Kuehn (MBio, 2016), which shows how gram-negative bacteria maintain the barrier properties of the outer membrane (OM) in a wide array of physiological conditions despite their inability to degrade lipopolysaccharide (LPS) and protein material present in the outer leaflet of the OM.

The tug-of-war over MTOR in Legionella infections

January 30, 2017

This article comments on work published by Abshire et al (PLoS Pathog, 2016), which uncovered that the host metabolic checkpoint kinase Mechanistic target of rapamycin (MTOR) is a central regulator of the pathogen niche expansion program.

A new role for Holliday junction resolvase Yen1 in processing DNA replication intermediates exposes Dna2 as an accessory replicative helicase

January 2, 2017

This article comments on work published by Ölmezer et al. (Nat Commun, 2016), which revealed a new function of Yen1, distinct from its previously known role as a Holliday junction resolvase, mediating the removal of branched HR intermediates.

Previous Next