Research, Research Articles

Knocking out histidine ammonia-lyase by using CRISPR-Cas9 abolishes histidine role in the bioenergetics and the life cycle of <i>Trypanosoma cruzi</i>

Knocking out histidine ammonia-lyase by using CRISPR-Cas9 abolishes histidine role in the bioenergetics and the life cycle of Trypanosoma cruzi

Janaína de Freitas Nascimento1, María Julia Barisón1, Gabriela Torres Montanaro1, Letícia Marchese1, Rodolpho Ornitz Oliveira Souza1, Letícia Sophia Silva2, Alessandra Aparecida Guarnieri2 and Ariel Mariano Silber1

Recent studies have highlighted the importance of this pathway in ATP production, redox balance, and the maintenance of cellular homeostasis in T. cruzi. In this work, we focus on the first step of the histidine degradation pathway, which is performed by the enzyme histidine ammonia lyase. Here we determined the kinetic and biochemical parameters of the T. cruzi histidine ammonia-lyase.

Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast

Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast

John-Patrick Alao1, Juhi Kumar1, Despina Stamataki2 and Charalampos Rallis1

Our findings show that caffeine accelerates mitotic division and is beneficial for CLS through AMPK. Direct pharmacological targeting of AMPK may serve towards healthspan and lifespan benefits beyond yeasts, given the highly conserved nature of this key regulatory cellular energy sensor.

Uga3 influences nitrogen metabolism in <i>Saccharomyces cerevisiae</i> by modulating arginine biosynthesis

Uga3 influences nitrogen metabolism in Saccharomyces cerevisiae by modulating arginine biosynthesis

Nicolás Urtasun1,2,a, Sebastián Aníbal Muñoz1,a, Martín Arán3 and Mariana Bermúdez-Moretti1

Nitrogen metabolism in Saccharomyces cerevisiae is tightly regulated to optimize the utilization of available nitrogen sources. Uga3 is a known transcription factor involved in the gamma-aminobutyric acid (GABA) pathway; however, its broader role in nitrogen metabolism remains unclear.

An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases

An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases

Sangeun Park, Sei-Kyoung Park, Peter Blair and Susan W. Liebman

This work offers new insights into the potential interactions between me-tabolite-based amyloids and pathological protein aggregates, with broad implications for understanding protein misfolding diseases.

Microbiota and metabolome dynamics induced by Shiga toxin-producing <i>E. coli</i> in an <i>in vitro</i> model of an infant’s colon

Microbiota and metabolome dynamics induced by Shiga toxin-producing E. coli in an in vitro model of an infant’s colon

Mariana Izquierdo1,a, Deborah O’Sullivan2,a, Ophélie Uriot2, Morgane Brun2, Claude Durif2, Sylvain Denis2, Pablo Gallardo1, Cormac G M Gahan3-5, Lucie Etienne-Mesmin2, Stéphanie Blanquet-Diot2,b and Mauricio J. Farfan1.b

This study provides new evidence of the impact of EHEC in the microbiota and metabolome dynamics in an in vitro gut model that could be useful in understanding their physiopathology in this at-risk population, considering inter-individual variabilities in gut microbiota.

Ampicillin treatment in persister cell studies may cause non-physiological artifacts

Ampicillin treatment in persister cell studies may cause non-physiological artifacts

Michel Fasnacht1,2, Hena Comic1,2, Isabella Moll1,2

This study shows at the example of L2 how insufficient purification of ampicillin persister cells can lead to the generation of non-physiological artifacts and provides a novel tool to improve the removal of residual cell debris.

<i>Clostridium scindens</i> promotes gallstone formation by inducing intrahepatic neutrophil extracellular traps through CXCL1 produced by colonic epithelial cells

Clostridium scindens promotes gallstone formation by inducing intrahepatic neutrophil extracellular traps through CXCL1 produced by colonic epithelial cells

Wenchao Yao1,a, Yuanhang He2,3,a, Zhihong Xie2,3, Qiang Wang2,3, Yang Chen2,4, Jingjing Yu2,3, Xuxu Liu2,3, Dongbo Xue2,3 , Liyi Wang2,3 and Chenjun Hao2,3

Through in vivo and in vitro experiments, we validated the reliability of C. scindens stimulating colonic epithelial cells to produce TLR2, activating the NF-κB signaling pathway, promoting CXCL1 expres-sion, and inducing intrahepatic neutrophil NETosis, which may be associated with gallstone formation.

Integrative Omics reveals changes in the cellular landscape of peroxisome-deficient <i>pex3</i> yeast cells

Integrative Omics reveals changes in the cellular landscape of peroxisome-deficient pex3 yeast cells

Tjasa Kosir1,a, Hirak Das2,a, Marc Pilegaard Pedersen1, Ann-Kathrin Richard2, Marco Anteghini3,4, Vitor Martins dos Santos4,5, Silke Oeljeklaus2, Ida J. van der Klei1 and Bettina Warscheid2

To uncover the consequences of peroxisome deficiency, we compared Saccharomyces cerevisiae wild-type with pex3 cells, which lack peroxisomes, employing quantitative proteomics and transcriptomics technologies.

Microwave-assisted preparation of yeast cells for ultrastructural analysis by electron microscopy

Microwave-assisted preparation of yeast cells for ultrastructural analysis by electron microscopy

Moritz Mayera, Christina Schuga, Stefan Geimer, Till Klecker and Benedikt Westermann

Budding yeast Saccharomyces cerevisiae is widely used as a model organism to study the biogenesis and architecture of organellar membranes, which can be visualized by transmission electron microscopy (TEM).

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Promoter methylation and increased expression of PD-L1 in patients with active tuberculosis

July 29, 2024

The PD-1/PD-L1 pathway plays a pivotal role in T cell activity and is involved in the pathophysiology of tuberculosis. Here we show that PD-L1 expression is increased in patients with active tuberculosis and is correlated with treatment outcomes.

Quantification methods of Candida albicans are independent irrespective of fungal morphology

July 26, 2024

Our study demonstrated that the quantification methods of C. albicans (cells/mL, CFU/mL, and vPCR) did not agree, regardless of the fungal morphology/growth, even though a significant and strong correlation is observed.

Pathogenic Escherichia coli change the adhesion between neutrophils and endotheliocytes in the experimental bacteremia model

July 22, 2024

In this work, we have demonstrated that in the model of experimental septicemia there is a disruption of adhesion contacts between neutrophils and endothelial cells, manifested by a decrease in adhesion force and work upon exposure to E. coli.

Arsenite treatment induces Hsp90 aggregates distinct from conventional stress granules in fission yeast

July 19, 2024

Given the conserved role of Hsp90 as a molecular chaperone protein, our findings presented in this study may suggest a novel type of arsenite-induced biological condensates, wherein Hsp90 plays a key role in maintaining its integrity.

Unresolved mystery of cyclic nucleotide second messengers, periplasmic acid phosphatases and bacterial natural competence

July 18, 2024

In this study we aimed to identify the promotors responsible for the expression of the non-specific acid phosphatase AphA during different starvation conditions, to confirm the requirement of the cAMP-dependent CRP regulon for aphA expression, and to finally identify regulators of its expression.

Expansion of metabolically labelled endocytic organelles and cytoskeletal cell structures in Giardia lamblia using optimised U- ExM protocols

June 21, 2024

Understanding cellular ultrastructure is tightly bound to microscopic resolution and the ability to identify individual components at that resolution. In this study we demonstrate mostly isotropic 4.5-fold expansion of several different compartments in Giardia cells and present an optimised, shortened, and modular protocol that can be swiftly adjusted to the investigators needs.

Polyadenylated versions of small non-coding RNAs in Saccharomyces cerevisiae are degraded by Rrp6p/Rrp47p independent of the core nuclear exosome

May 22, 2024

In this investigation, we unveiled a novel functional role of the major nuclear 3′→5′ exoribonuclease, Rrp6p, and its cofactor Rrp47p in the degradation of polyadenylated versions of several mature sncRNAs, including 5S, 5.8S rRNAs, all sn- and some select snoRNAs in the baker’s yeast S. cerevisiae.

Exploring carbon source related localization and phosphorylation in the Snf1/Mig1 network using population and single cell-based approaches

May 16, 2024

In this work we set out to explore the relationship between the subcellular localization and regulation of kinases in the context of carbon source signaling. The data presented in this paper reinforce the notion that not only the activation/inactivation of kinases but also their subcellular localization and that of their targets influence fate decisions in response to environmental changes.

A Modular Cloning Toolkit for the production of recombinant proteins in Leishmania tarentolae

April 30, 2024

Modular Cloning (MoClo) is based on libraries of standardized genetic parts that can be directionally assembled via Golden Gate cloning in one-pot reactions into transcription units and multigene constructs. We established a MoClo toolkit and exemplified its application for the production of recombinant proteins in L. tarentolae.

A metagenomic approach to unveil the association between fecal gut microbiota and short-chain fatty acids in diarrhea caused by diarrheagenic Escherichia coli in children

April 30, 2024

Diarrheagenic Escherichia coli (DEC) is the main cause of diarrhea in children under five years old. The virulence of DEC is tightly regulated by environmental signals influenced by the gut microbiota and its metabolites. Our results increase the knowledge of the association between short chain fatty acids during diarrhea and changes in the microbiota composition associated with the presence of DEC pathogens.

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