Review, Reviews

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

Gonorrhea – an evolving disease of the new millennium

September 4, 2016

Neisseria gonorrhoeae (the gonococcus) is a Gram-negative diplococcus, an obligate human pathogen, and the etiologic agent of the sexually transmitted disease, gonorrhea. This review provides insight into the molecular epidemiology, virulence mechanisms, pathogenesis and therapeutic options.

Functions and regulation of the MRX complex at DNA double-strand breaks

July 27, 2016

DNA double-strand breaks (DSBs) pose a serious threat to genome stability and cell survival. Cells possess mechanisms that recognize DSBs and promote their repair through either homologous recombination (HR) or non-homologous end joining (NHEJ). The present review focuses mainly on recent works in the budding yeast Saccharomyces cerevisiae to highlight structure and regulation of the evolutionary conserved Mre11-Rad50-Xrs2 (MRX) complex as well as its interplays with Tel1.

Syphilis: Re-emergence of an old foe

June 27, 2016

Syphilis is caused by infection with Treponema pallidum subsp. pallidum, a not-yet-cultivable spiral-shaped bacterium that is usually transmitted by sexual contact with an infected partner or by an infected pregnant woman to her fetus. This review provides insights into the etiology, epidemiology, clinical manifestation, diagnosis, treatment and prevention of syphilis.

Genital Herpes: Insights into Sexually Transmitted Infectious Disease

June 27, 2016

Genital herpes is one of the most common, persistent and highly infectious sexually transmitted viral infections. This review provides an insight into the epidemiology, pathology, our current understanding of the molecular mechanisms of infection and the currently available and upcoming treatments for genital herpes.

Trichomoniasis – are we giving the deserved attention to the most common non-viral sexually transmitted disease worldwide?

June 27, 2016

Trichomonas vaginalis is the etiologic agent of trichomoniasis, the most common non-viral sexually transmitted disease (STD) in the world. This article contributes to claim the attention of public health policies to control this STD.

Evidence for the hallmarks of human aging in replicatively aging yeast

June 20, 2016

Recently, efforts have been made to characterize the hallmarks that accompany and contribute to the phenomenon of aging, as most relevant for humans. Remarkably, studying the finite lifespan of the single cell eukaryote budding yeast has been paramount for our understanding of aging. Here, we compile observations from literature over the past decades of research on replicatively aging yeast to highlight how the hallmarks of aging in humans are present in yeast.

The molecular and cellular action properties of artemisinins: what has yeast told us?

April 14, 2016

Artemisinin (ART) or Qinghaosu is a natural compound possessing superior anti-malarial activity. Although intensive studies have been done in the medicinal chemistry field to understand the structure-effect relationship, the biological actions of artemisinin are poorly understood and controversial. This review summarizes what we have learned from yeast about the basic biological properties of ARTs, as well as some key unanswered questions.

Chromatin binding and silencing: Two roles of the same protein Lem2

April 4, 2016

This article comments on work published by Barrales et al. (Genes Dev, 2016), which identifies the nuclear envelope protein Lem2, a homolog of metazoan lamin-associated proteins (LAPs), as a relevant factor for heterochromatin silencing and perinuclear localization in the fission yeast Schizosaccharomyces pombe.

Signaling pathways and posttranslational modifications of tau in Alzheimer’s disease: the humanization of yeast cells

March 27, 2016

In the past decade, yeast have been frequently employed to study the molecular mechanisms of human neurodegenerative diseases, generally by means of heterologous expression of genes encoding the relevant hallmark proteins. Substantial posttranslational modifications of many of these proteins are required for the development and progression of potentially disease relevant changes. We give an overview on common modifications as they occur in tau during AD and discuss potential approaches to humanize yeast in order to create modification patterns resembling the situation in mammalian cells.

Histone modifications as regulators of life and death in Saccharomyces cerevisiae

December 31, 2015

The mechanism by which chromosomes restructure during apoptosis is still poorly understood, but it is becoming increasingly clear that altered epigenetic histone modifications are fundamental parameters that influence the chromatin state and the nuclear rearrangements within apoptotic cells. This review highlights recent work on the epigenetic regulation of programmed cell death in budding yeast.

Previous Next