Microreviews, Review

Placeholder factors in ribosome biogenesis: please, pave my way

Francisco J. Espinar-Marchena, Reyes Babiano1 and Jesús de la Cruz

In ribosome synthesis, "placeholder" factors are crucial trans-acting elements that regulate the timing and assembly of ribosomal proteins, ensuring speed and accuracy in this intricate process by preventing premature interactions and guiding the proper formation of functional ribosomal subunits.

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

Hong Li1,2, Tiandi Yang3, Tingting Liao2, Aleksandra W. Debowski2,4, Hans-Olof Nilsson2, Stuart M. Haslam3, Anne Dell3, Keith A. Stubbs4, Barry J. Marshall2 and Mohammed Benghezal2,5

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

Christopher Waite1, Jörg Schumacher1, Milija Jovanovic1, Mark Bennett1 and Martin Buck1

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

Facundo Rodriguez Ayala, Carlos Bauman, Sebastián Cogliati, Cecilia Leñini, Marco Bartolini and Roberto Grau

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

Barbara S. Sixt1-4, Raphael H. Valdivia5, Guido Kroemer1-4,6-7

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

Tâm Mignot1 and Marcelo Nöllmann2

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

Chul-Su Yang

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

Katherine E. Bonnington, Meta J. Kuehn

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

Stanimir S. Ivanov

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.

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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.

Toxin-mediated gene regulatory mechanism in Staphylococcus aureus

December 29, 2016

This article comments on work published by Joo et al. (MBio, 2016), which describes the first molecular regulatory mechanism exerted by an S. aureus toxin, setting a paradigmatic example of how S. aureus toxins may influence cell functions to adjust them to times of toxin production.

Autophagy: machinery and regulation

December 1, 2016

Macroautophagy/autophagy is an evolutionarily conserved cellular degradation process that targets cytoplasmic materials including cytosol, macromolecules and unwanted organelles. The discovery and analysis of autophagy-related (Atg) proteins have unveiled much of the machinery of autophagosome formation. In this review, we briefly summarize the physiological roles, molecular mechanism, regulatory network, and pathophysiological roles of autophagy.

NprR, a moonlighting quorum sensor shifting from a phosphatase activity to a transcriptional activator

November 5, 2016

This article comments on work published by Perchat et al. (PLoS Pathog, 2016), which demonstrates that, in the absence of the signaling peptide NprX, the sensor NprR is a dimer, which negatively controls sporulation in Bacillus thuringiensis, independently of its transcription factor activity.

Threading Granules in Freiburg: 2nd International Symposium on “One Mitochondrion, Many Diseases – Biological and Molecular Perspectives”, a FRIAS Junior Researcher Conference, Freiburg im Breisgau, Germany, March 9th/10th, 2016

November 4, 2016

INTRODUCTION Mitochondria (greek: μίτος & χονδρίον, mitos & chondrion, i.e., thread & granule) are the power houses of eukaryotic cells, and are pivotally involved in essential metabolic processes, including iron/sulfur cluster and heme ... Read more

The interaction between herpes simplex virus 1 genome and promyelocytic leukemia nuclear bodies (PML-NBs) as a hallmark of the entry in latency

November 4, 2016

This article comments on work published by Maroul et al. (PLoS Pathog, 2016), which demonstrates that the interaction of the viral genomes with the nuclear architecture and specifically the promyelocytic leukemia nuclear bodies is a major determinant for the entry of HSV-1 into latency.

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