Strain phylogroup and environmental constraints shape Escherichia coli dynamics and diversity over a twenty-year human gut time series.

Escherichia coli is an increasingly antibiotic-resistant opportunistic pathogen. Few data are available on its ecological and evolutionary dynamics in its primary commensal niche, the vertebrate gut. Using Illumina and/or Nanopore technologies, we sequenced whole genomes of 210 E.

Exploring the diversity of anti-defense systems across prokaryotes, phages and mobile genetic elements.

The co-evolution of prokaryotes, phages and mobile genetic elements (MGEs) has driven the diversification of defense and anti-defense systems alike. Anti-defense proteins have diverse functional domains, sequences and are typically small, creating a challenge to detect anti-defense homologs across prokaryotic and phage genomes. To date, no tools comprehensively annotate anti-defense proteins within a desired sequence.

Prediction of strain level phage-host interactions across the Escherichia genus using only genomic information.

Predicting bacteriophage infection of specific bacterial strains promises advancements in phage therapy and microbial ecology. Whether the dynamics of well-established phage-host model systems generalize to the wide diversity of microbes is currently unknown. Here we show that we could accurately predict the outcomes of phage-bacteria interactions at the strain level in natural isolates from the genus Escherichia using only genomic data (area under the receiver operating characteristic curve (AUROC) of 86%).

A virally encoded tRNA neutralizes the PARIS antiviral defence system.

Viruses compete with each other for limited cellular resources, and some deliver defence mechanisms that protect the host from competing genetic parasites. The phage antirestriction induced system (PARIS) is a defence system, often encoded in viral genomes, that is composed of a 55 kDa ABC ATPase (AriA) and a 35 kDa TOPRIM nuclease (AriB). However, the mechanism by which AriA and AriB function in phage defence is unknown.

Genome sequence and characterization of Streptomyces phages Vanseggelen and Verabelle, representing two new species within the genus Camvirus.

Despite the rising interest in bacteriophages, little is known about their infection cycle and lifestyle in a multicellular host. Even in the model system Streptomyces, only a small number of phages have been sequenced and well characterized so far. Here, we report the complete characterization and genome sequences of Streptomyces phages Vanseggelen and Verabelle isolated using Streptomyces coelicolor as a host.

Genomic characterization of the antiviral arsenal of Actinobacteria.

Phages are ubiquitous in nature, and bacteria with very different genomics, metabolisms, and lifestyles are subjected to their predation. Yet, the defence systems that allow bacteria to resist their phages have rarely been explored experimentally outside a very limited number of model organisms. Actinobacteria (Actinomycetota) are a phylum of GC-rich Gram-positive bacteria, which often produce an important diversity of secondary metabolites.

Synergy and regulation of antiphage systems: toward the existence of a bacterial immune system?

Bacteria encode a vast repertoire of diverse antiphage defense systems. Recent studies revealed that different defense systems are often encoded within the same genome, raising the question of their possible interactions in a cell. Here, we review the known synergies and coregulations of antiphage systems.

Systematic and quantitative view of the antiviral arsenal of prokaryotes.

Bacteria and archaea have developed multiple antiviral mechanisms, and genomic evidence indicates that several of these antiviral systems co-occur in the same strain. Here, we introduce DefenseFinder, a tool that automatically detects known antiviral systems in prokaryotic genomes. We use DefenseFinder to analyse 21000 fully sequenced prokaryotic genomes, and find that antiviral strategies vary drastically between phyla, species and strains.

A CRISPR/Cas9 zebrafish lamin A/C mutant model of muscular laminopathy.

Background: Lamin A/C gene (LMNA) mutations frequently cause cardiac and/or skeletal muscle diseases called striated muscle laminopathies. We created a zebrafish muscular laminopathy model using CRISPR/Cas9 technology to target the zebrafish lmna gene.

Results: Heterozygous and homozygous lmna mutants present skeletal muscle damage at 1 day post-fertilization (dpf), and mobility impairment at 4 to 7 dpf.

Belief and adherence to COVID 19-lockdown restrictions in patients with asthma versus other chronic diseases: results from a cross-sectional survey nested in the ComPaRe e-cohort, in France.

Background: Asthma patients are under-represented among patients with COVID-19. Their behavior during lockdown and associated restrictions is unknown, as well as whether it was influenced by coexistent cardiovascular conditions.

Methods: We conducted a cross-sectional survey in May 2020, in France, nested in ComPaRe, an e-cohort of adults with chronic diseases.

Protein Kinase C Alpha Cellular Distribution, Activity, and Proximity with Lamin A/C in Striated Muscle Laminopathies.

Striated muscle laminopathies are cardiac and skeletal muscle conditions caused by mutations in the lamin A/C gene (). codes for the A-type lamins, which are nuclear intermediate filaments that maintain the nuclear structure and nuclear processes such as gene expression. Protein kinase C alpha (PKC-α) interacts with lamin A/C and with several lamin A/C partners involved in striated muscle laminopathies.

Can Circulating Cardiac Biomarkers Be Helpful in the Assessment of Mutation Carriers?

Mutations in the lamin A/C gene are variably phenotypically expressed; however, it is unclear whether circulating cardiac biomarkers are helpful in the detection and risk assessment of cardiolaminopathies. We sought to assess (1) clinical characteristics including serum biomarkers: high sensitivity troponin T (hsTnT) and N-terminal prohormone brain natriuretic peptide (NT-proBNP) in clinically stable cardiolaminopathy patients, and (2) outcome among pathogenic/likely pathogenic lamin A/C gene ( mutation carriers. Our single-centre cohort included 53 patients from 21 families.

Cellular and Animal Models of Striated Muscle Laminopathies.

The lamin A/C () gene codes for nuclear intermediate filaments constitutive of the nuclear lamina. has 12 exons and alternative splicing of exon 10 results in two major isoforms-lamins A and C. Mutations found throughout the gene cause a group of diseases collectively known as laminopathies, of which the type, diversity, penetrance and severity of phenotypes can vary from one individual to the other, even between individuals carrying the same mutation.

ACSL5 genotype influence on fatty acid metabolism: a cellular, tissue, and whole-body study.

Background: Acyl-CoA Synthetase Long Chain 5 (ACSL5) gene's rs2419621 T/C polymorphism was associated with ACSL5 mRNA expression and response to lifestyle interventions. However, the mechanistic understanding of the increased response in T allele carriers is lacking. Study objectives were to investigate the effect of rs2419621 genotype and ACSL5 human protein isoforms on fatty acid oxidation and respiration.

Acyl-CoA synthetase long-chain 5 genotype is associated with body composition changes in response to lifestyle interventions in postmenopausal women with overweight and obesity: a genetic association study on cohorts Montréal-Ottawa New Emerging Team, and Complications Associated with Obesity.

Background: Genetic studies on Acyl-CoA Synthetase Long-Chain 5 (ACSL5) demonstrate an association between rs2419621 genotype and rate of weight loss in women with obesity in response to caloric restriction. Our objectives were to (1) confirm results in two different populations of women with overweight and obesity (2) study rs2419621's influence on body composition parameters of women with overweight and obesity following lifestyle interventions.

Methods: rs2419621 genotype was determined in women with overweight and obesity who participated in the Montréal-Ottawa New Emerging Team (MONET n = 137) and Complications Associated with Obesity (CAO n = 37) studies.

Lamin A/C mutations in dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is one of the leading causes of heart failure and heart transplant. Mutations in 60 genes have been associated with DCM. Approximately 6% of all DCM cases are caused by mutations in the lamin A/C gene (LMNA).

LMNA mutations in Polish patients with dilated cardiomyopathy: prevalence, clinical characteristics, and in vitro studies.

Background: LMNA mutations are most frequently involved in the pathogenesis of dilated cardiomyopathy with conduction disease. The goal of this study was to identify LMNA mutations, estimate their frequency among Polish dilated cardiomyopathy patients and characterize their effect both in vivo and in vitro.

Methods: Between January, 2008 and June, 2012 two patient populations were screened for the presence of LMNA mutations by direct sequencing: 66 dilated cardiomyopathy patients including 27 heart transplant recipients and 39 dilated cardiomyopathy patients with heart failure referred for heart transplantation evaluation, and 44 consecutive dilated cardiomyopathy patients, referred for a family evaluation and mutation screening.

The TaqIA RFLP is associated with attenuated intervention-induced body weight loss and increased carbohydrate intake in post-menopausal obese women.

Introduction: Polymorphisms of the dopamine receptor D2 (DRD2) gene have been associated with obesity phenotypes. Our aim was to examine if the genotype of TaqIA Restriction Fragment Length Polymorphism (RFPL) was related to an attenuated weight loss response or to changes in energy expenditure (EE) and food preference before and after weight loss. methods: Obese post-menopausal women (age=57.

Lamin A/C mutants disturb sumo1 localization and sumoylation in vitro and in vivo.

A-type lamins A and C are nuclear intermediate filament proteins in which mutations have been implicated in multiple disease phenotypes commonly known as laminopathies. A few studies have implicated sumoylation in the regulation of A-type lamins. Sumoylation is a post-translational protein modification that regulates a wide range of cellular processes through the attachment of small ubiquitin-related modifier (sumo) to various substrates.

Variants of the lamin A/C (LMNA) gene in non-valvular atrial fibrillation patients: a possible pathogenic role of the Thr528Met mutation.

Background And Objective: Lamin A/C (LMNA) gene mutations cause dilated cardiomyopathy, often accompanied by conduction disturbances. Our aim was to search for LMNA mutations in individuals with atrial fibrillation.

Methods: A cohort of Polish subjects (N = 103) with non-valvular atrial fibrillation with a high (48.