Grids of stellar models with rotation - III. Models from 0.8 to 120 Msun at a metallicity Z = 0.002

(shortened) We provide a grid of single star models covering a mass range from 0.8 to 120 Msun with an initial metallicity Z = 0.002 with and without rotation. We discuss the impact of a change in the metallicity by comparing the current tracks with models computed with exactly the same physical ingredients but with a metallicity Z = 0.014 (solar). We show that the width of the main-sequence (MS) band in the upper part of the Hertzsprung-Russell diagram (HRD), for luminosity above log(L/Lsun) > 5.5, is very sensitive to rotational mixing. Strong mixing significantly reduces the MS width. We confirm, but here for the first time on the whole mass range, that surface enrichments are stronger at low metallicity provided that comparisons are made for equivalent initial mass, rotation and evolutionary stage. We show that the enhancement factor due to a lowering of the metallicity (all other factors kept constant) increases when the initial mass decreases. Present models predict an upper luminosity for the red supergiants (RSG) of log (L/Lsun) around 5.5 at Z = 0.002 in agreement with the observed upper limit of RSG in the Small Magellanic Cloud. We show that models using shear diffusion coefficient calibrated to reproduce the surface enrichments observed for MS B-type stars at Z = 0.014 can also reproduce the stronger enrichments observed at low metallicity. In the framework of the present models, we discuss the factors governing the timescale of the first crossing of the Hertzsprung gap after the MS phase. We show that any process favouring a deep localisation of the H-burning shell (steep gradient at the border of the H-burning convective core, low CNO content) and/or the low opacity of the H-rich envelope favour a blue position in the HRD for the whole or at least a significant fraction of the core He-burning phase.Comment: 17 pages, 15 figures, 2 tables. Accepted for publication in Astronomy and Astrophysic

Évaluation de l'efficacité de la lithotripsie extracorporelle pour les calculs rénaux de plus de 20 millimètres

INTRODUCTION : Les calculs rénaux de plus de 20 millimètres (mm) nécessitent une prise en charge. La lithotripsie extracorporelle est une procédure peu invasive avec peu de morbidité. Les recommandations préconisent la réalisation d’une néphrolithotomie per cutanée en première intention. L’objectif principal de l’étude était d’évaluer l’efficacité de la lithotripsie pour les calculs rénaux de plus de 20mm.MATÉRIELS ET MÉTHODES : Étude observationnelle rétrospective, monocentrique, de 105 patients inclus entre 2014 et 2018. Les tests étaient bilatéraux et une p-value<5% était considérée statistiquement significative.RÉSULTATS : La taille moyenne des lithiases était de 29,39mm. La densité moyenne des calculs était de 880 unités Hounsfield. Le nombre moyen de coups par séance était de 3507. Le nombre moyen de séance était de 4,05. Le taux d’efficacité, absence de fragment résiduel et fragment inférieur ou égal à 4mm était de 68%. Il a été retrouvé une meilleure efficacité pour les calculs de faible densité. Cette série comportait 24% de colique néphrétique post procédure, 11% de pyélonéphrite obstructive, 16% de pose de sonde double J. Le nombre de coups par séance n’était pas en lien avec les complications. La mise en place de sonde double J avant la lithotripsie avait permis une diminution du nombre de colique néphrétique.CONCLUSION : Cette étude avait mis en évidence un taux de réussite de 68% sous condition d’effectuer plusieurs séances avec une morbidité majorée de ce fait. Ce taux de réussite est intéressant pour les patients poly-pathologiques dont l’anesthésie est à risque

Xrcc1-dependent and Ku-dependent DNA double-strand break repair kinetics in Arabidopsis plants.

International audienceDouble-strand breakage (DSB) of DNA involves loss of information on the two strands of the DNA fibre and thus cannot be repaired by simple copying of the complementary strand which is possible with single-strand DNA damage. Homologous recombination (HR) can precisely repair DSB using another copy of the genome as template and non-homologous recombination (NHR) permits repair of DSB with little or no dependence on DNA sequence homology. In addition to the well-characterised Ku-dependent non-homologous end-joining (NHEJ) pathway, much recent attention has been focused on Ku-independent NHR. The complex interrelationships and regulation of NHR pathways remain poorly understood, even more so in the case of plants, and we present here an analysis of Ku-dependent and Ku-independent repair of DSB in Arabidopsis thaliana. We have characterised an Arabidopsis xrcc1 mutant and developed quantitative analysis of the kinetics of appearance and loss of γ-H2AX foci as a tool to measure DSB repair in dividing root tip cells of γ-irradiated plants in vivo. This approach has permitted determination of DSB repair kinetics in planta following a short pulse of γ-irradiation, establishing the existence of a Ku-independent, Xrcc1-dependent DSB repair pathway. Furthermore, our data show a role for Ku80 during the first minutes post-irradiation and that Xrcc1 also plays such a role, but only in the absence of Ku. The importance of Xrcc1 is, however, clearly visible at later times in the presence of Ku, showing that alternative end-joining plays an important role in DSB repair even in the presence of active NHEJ

Kinetic analysis of DNA double-strand break repair pathways in Arabidopsis.

International audienceDouble-strand breaks in genomic DNA (DSB) are potentially lethal lesions which separate parts of chromosome arms from their centromeres. Repair of DSB by recombination can generate mutations and further chromosomal rearrangements, making the regulation of recombination and the choice of recombination pathways of the highest importance. Although knowledge of recombination mechanisms has considerably advanced, the complex interrelationships and regulation of pathways are far from being fully understood. We analyse the different pathways of DSB repair acting in G2/M phase nuclei of irradiated plants, through quantitation of the kinetics of appearance and loss of γ-H2AX foci in Arabidopsis mutants. These analyses show the roles for the four major recombination pathways in post-S-phase DSB repair and that non-homologous recombination pathways constitute the major response. The data suggest a hierarchical organisation of DSB repair in these cells: C-NHEJ acts prior to B-NHEJ which can also inhibit MMEJ. Surprisingly the quadruple ku80 xrcc1 xrcc2 xpf mutant can repair DSB, although with severely altered kinetics. This repair leads to massive genetic instability with more than 50% of mitoses showing anaphase bridges following irradiation. This study thus clarifies the relationships between the different pathways of DSB repair in the living plant and points to the existence of novel DSB repair processes

RAD51 and RTEL1 compensate telomere loss in the absence of telomerase

International audienceReplicative erosion of telomeres is naturally compensated by telomerase and studies in yeast and vertebrates show that homologous recombination can compensate for the absence of telomerase. We show that RAD51 protein, which catalyzes the key strand-invasion step of homologous recombination, is localized at Arabidopsis telomeres in absence of telomerase. Blocking the strand-transfer activity of the RAD51 in telomerase mutant plants results in a strikingly earlier onset of developmental defects, accompanied by increased numbers of end-to-end chromosome fusions. Imposing replication stress through knockout of RNaseH2 increases numbers of chromosome fusions and reduces the survival of these plants deficient for telomerase and homologous recombination. This finding suggests that RAD51-dependent homologous recombination acts as an essential backup to the telomerase for compensation of replicative telomere loss to ensure genome stability. Furthermore, we show that this positive role of RAD51 in telomere stability is dependent on the RTEL1 helicase. We propose that a RAD51 dependent break-induced replication process is activated in cells lacking telomerase activity, with RTEL1 responsible for D-loop dissolution after telomere replication

Colonization and immune modulation properties of Klebsiella pneumoniae biofilm-dispersed cells

Biofilm-dispersal is a key determinant for further dissemination of biofilm-embedded bacteria. Recent evidence indicates that biofilm-dispersed bacteria have transcriptional features different from those of both biofilm and planktonic bacteria. In this study, the in vitro and in vivo phenotypic properties of Klebsiella pneumoniae cells spontaneously dispersed from biofilm were compared with those of planktonic and sessile cells. Biofilm-dispersed cells, whose growth rate was the same as that of exponential planktonic bacteria but significantly higher than those of sessile and stationary planktonic forms, colonized both abiotic and biotic surfaces more efficiently than their planktonic counterparts regardless of their initial adhesion capabilities. Microscopy studies suggested that dispersed bacteria initiate formation of microcolonies more rapidly than planktonic bacteria. In addition, dispersed cells have both a higher engulfment rate and better survival/multiplication inside macrophages than planktonic cells and sessile cells. In an in vivo murine pneumonia model, the bacterial load in mice lungs infected with biofilm-dispersed bacteria was similar at 6, 24 and 48 h after infection to that of mice lungs infected with planktonic or sessile bacteria. However, biofilm-dispersed and sessile bacteria trend to elicit innate immune response in lungs to a lesser extent than planktonic bacteria. Collectively, the findings from this study suggest that the greater ability of K. pneumoniae biofilm-dispersed cells to efficiently achieve surface colonization and to subvert the host immune response confers them substantial advantages in the first steps of the infection process over planktonic bacteria

Transcriptional profiling of Klebsiella pneumoniae defines signatures for planktonic, sessile and biofilm-dispersed cells

International audienceBackgroundSurface-associated communities of bacteria, known as biofilms, play a critical role in the persistence and dissemination of bacteria in various environments. Biofilm development is a sequential dynamic process from an initial bacterial adhesion to a three-dimensional structure formation, and a subsequent bacterial dispersion. Transitions between these different modes of growth are governed by complex and partially known molecular pathways.ResultsUsing RNA-seq technology, our work provided an exhaustive overview of the transcriptomic behavior of the opportunistic pathogen Klebsiella pneumoniae derived from free-living, biofilm and biofilm-dispersed states. For each of these conditions, the combined use of Z-scores and principal component analysis provided a clear illustration of distinct expression profiles. In particular, biofilm-dispersed cells appeared as a unique stage in the bacteria lifecycle, different from both planktonic and sessile states. The K-means cluster analysis showed clusters of Coding DNA Sequences (CDS) and non-coding RNA (ncRNA) genes differentially transcribed between conditions. Most of them included dominant functional classes, emphasizing the transcriptional changes occurring in the course of K. pneumoniae lifestyle transitions. Furthermore, analysis of the whole transcriptome allowed the selection of an overall of 40 transcriptional signature genes for the five bacterial physiological states.ConclusionsThis transcriptional study provides additional clues to understand the key molecular mechanisms involved in the transition between biofilm and the free-living lifestyles, which represents an important challenge to control both beneficial and harmful biofilm. Moreover, this exhaustive study identified physiological state specific transcriptomic reference dataset useful for the research community

Distinct Roles of the ATR Kinase and the Mre11-Rad50-Nbs1 Complex in the Maintenance of Chromosomal Stability in Arabidopsis

DNA damage signaling of chromosomal DNA breaks is of primary importance for initiation of repair and, thus, for global genomic stability. This work confirms that the signaling of double-strand damage is conserved in plants and provides evidence for key roles of the MRN complex and ATR in assuring proper DNA replication in the absence of exogenously induced DNA damage

The linker histone GH1-HMGA1 is involved in telomere stability and DNA damage repair

International audienceDespite intensive searches, few proteins involved in telomere homeostasis have been identified in plants. Here, we used pull-down assays to identify potential telomeric interactors in the model plant species Arabidopsis (Arabidopsis thaliana). We identified the candidate protein GH1-HMGA1 (also known as HON4), an uncharacterized linker histone protein of the High Mobility Group Protein A (HMGA) family in plants. HMGAs are architectural transcription factors and have been suggested to function in DNA damage repair, but their precise biological roles remain unclear. Here, we show that GH1-HMGA1 is required for efficient DNA damage repair and telomere integrity in Arabidopsis. GH1-HMGA1 mutants exhibit developmental and growth defects, accompanied by ploidy defects, increased telomere dysfunction-induced foci, mitotic anaphase bridges, and degraded telomeres. Furthermore, mutants have a higher sensitivity to genotoxic agents such as mitomycin C and γ-irradiation. Our work also suggests that GH1-HMGA1 is involved directly in the repair process by allowing the completion of homologous recombination