Microreviews, Review

Where antibiotic resistance mutations meet quorum-sensing

Rok Krašovec1, Roman V. Belavkin2, John A.D. Aston3, Alastair Channon4, Elizabeth Aston4, Bharat M. Rash1, Manikandan Kadirvel5,6, Sarah Forbes6, and Christopher G. Knight1

This article comments on work published by Krašovec et al. (Nat Comm, 2014), which found that the modulation of de novo mutation to promote antibiotic resistance depends on the density of the bacterial population and cell-cell interactions (rather than, for instance, the level of stress).

Sphingolipids and mitochondrial function, lessons learned from yeast

Pieter Spincemaille1, Bruno P.A. Cammue1,2 and Karin Thevissen1

This article reviews recent research showing that Saccharomyces cerevisiae is an invaluable model to investigate sphingolipids as signaling molecules in modulating mitochondrial function, but can also be used as a tool to further enhance our current knowledge on sphingolipids and mitochondria in mammalian cells.

Genome evolution in yeast reveals connections between rare mutations in human cancer

Xinchen Teng1,2 and J. Marie Hardwick2

This article comments on work published by Teng et al. (Mol Cell, 2013), which, using the yeast knockout collections, provides hard evidence that single gene deletions/mutations in most non-essential genes can drive the selection for cancer-like mutations.

Cell-autonomous mechanisms of chronological aging in the yeast Saccharomyces cerevisiae

Anthony Arlia-Ciommo#, Anna Leonov#, Amanda Piano#, Veronika Svistkova# and Vladimir I. Titorenko

This article critically analyzes recent advances in the understanding of cell-autonomous mechanisms of chronological aging in the budding yeast Saccharomyces cerevisiae. It proposes a concept of a biomolecular network underlying the chronology of cellular aging in yeast, whichposits that such network progresses through a series of lifespan checkpoints.

Decoding the biosynthesis and function of diphthamide, an enigmatic modification of translation elongation factor 2 (EF2)

Raffael Schaffrath and Michael J. R. Stark

This article comments on work published by Uthman et al. (PLoS Genet, 2013), which suggests that Dph5 has a novel role as an EF2 inhibitor that affects cell growth when diphthamide synthesis is blocked or incomplete and shows that diphthamide promotes the accuracy of EF2 performance during translation.

Autophagy extends lifespan via vacuolar acidification

Christoph Ruckenstuhl1, Christine Netzberger1, Iryna Entfellner1, Didac Carmona-Gutierrez1, Thomas Kickenweiz1, Slaven Stekovic1, Christina Gleixner1, Christian Schmid1, Lisa Klug1, Ivan Hajnal1, Alice G. Sorgo1, Tobias Eisenberg1, Sabrina Büttner1, Guillermo Marin͂o2-4,  Rafal Koziel5, Christoph Magnes6, Frank Sinner6,7, Thomas R. Pieber6,7, Pidder Jansen-Dürr5, Kai-Uwe Fröhlich1, Guido Kroemer2,3,8-11, and Frank Madeo1

This article comments on work published by Ruckenstuhl et al. (PLoS Genet, 2014), which uses Saccharomyces cerevisiae to show that autophagy promotes lifespan extension upon MetR and requires the subsequent stimulation of vacuolar acidification, while it is epistatic to the equally autophagy-dependent anti-aging pathway triggered by TOR1 inhibition or deletion.

When less is more: hormesis against stress and disease

Andreas Zimmermann1, Maria A. Bauer1, Guido Kroemer2-5, Frank Madeo1 and Didac Carmona-Gutierrez1

This article condenses the conceptual and potentially therapeutic importance of hormesis by providing a short overview of current evidence in favor of the cytoprotective impact of hormesis, as well as of its underlying molecular mechanisms.

Morphed and moving: TNFα-driven motility promotes cell dissemination through MAP4K4-induced cytoskeleton remodeling

Min Ma1,2 and Martin Baumgartner1

This article comments on work published by Ma and Baumgartner (PLoS Patho, 2014), which investigated Theileria parasite control of host cell motile properties in the context of inflammatory signaling.

Hormesis: a fundamental concept in biology

Edward J. Calabrese

This article addresses the concept of hormetic dose response, which describes the limits to which integrative endpoints can be modulated (i.e., enhanced or diminished) by pharmaceutical, chemical and physical means.

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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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