Contrasted Patterns of Molecular Evolution in Dominant and Recessive Self-Incompatibility Haplotypes in Arabidopsis

Self-incompatibility has been considered by geneticists a model system for reproductive biology and balancing selection, but our understanding of the genetic basis and evolution of this molecular lock-and-key system has remained limited by the extreme level of sequence divergence among haplotypes, resulting in a lack of appropriate genomic sequences. In this study, we report and analyze the full sequence of eleven distinct haplotypes of the self-incompatibility locus (S-locus) in two closely related Arabidopsis species, obtained from individual BAC libraries. We use this extensive dataset to highlight sharply contrasted patterns of molecular evolution of each of the two genes controlling self-incompatibility themselves, as well as of the genomic region surrounding them. We find strong collinearity of the flanking regions among haplotypes on each side of the S-locus together with high levels of sequence similarity. In contrast, the S-locus region itself shows spectacularly deep gene genealogies, high variability in size and gene organization, as well as complete absence of sequence similarity in intergenic sequences and striking accumulation of transposable elements. Of particular interest, we demonstrate that dominant and recessive S-haplotypes experience sharply contrasted patterns of molecular evolution. Indeed, dominant haplotypes exhibit larger size and a much higher density of transposable elements, being matched only by that in the centromere. Overall, these properties highlight that the S-locus presents many striking similarities with other regions involved in the determination of mating-types, such as sex chromosomes in animals or in plants, or the mating-type locus in fungi and green algae

Blade row interference and clocking effects in a one and half stage turbine

Ce travail de recherche, principalement expérimental, consiste en l étude et l analyse de l aérodynamique et du transfert thermique dans un étage et demi de turbine. Cette turbine est testé avec des nombres de Reynolds (106) et de Mach, ainsi que des rapports de température gaz/surface et gaz/refroidissant représentatifs de ceux d une turbine HP utilisée en aéronautique. Les mesures de pression et de flux chaleur ont été accomplies de manière à obtenir les composantes stationnaires et instationnaires de l écoulement. Une précédente étude réalisée au sein de l Institut von Karman s était intéressée aux interactions entre le distributeur amont et le rotor de l étage haute pression. La présente étude met en avant l interaction entre l étage haute pression et le second stator au travers de la caractérisation des effets de clocking. Les conclusions de cette étude peuvent être directement utilisées par les concepteurs pour optimiser le positionnement d un second stator en terme de rendement et de minimisation des fluctuations des efforts ou de la charge thermique appliqués par l écoulement sur l aubage.The present research, mostly experimental, consists in investigating and analyzing the aerodynamic and heat transfer in a one and half stage turbine. The turbine is tested under engine representative Reynolds number (106), Mach number (0.9), gas to wall temperature ratio (1.5) and gas to coolant temperature ratio (2.1). Pressure and heat flux measurements were performed in order to obtain both steady and unsteady components of the flow field. Previous investigations focused on the interaction between the inlet guide vane and the rotor of the high-pressure stage. The current work highlights the interaction between the high-pressure stage and the second stator by characterizing clocking effects. The findings of this study may be used by designers to optimiste the position of the second stator in terms of effieciency, blade force fluctuations or heat load minimization.LYON-Ecole Centrale (690812301) / SudocSudocFranceF

Identifying conversion efficiency as a key mechanism underlying food webs evolution: A step forward, or backward?

Body size or mass is generally seen as one of the main factors which structure food webs. A large number of evolutionary models have shown that indeed, the evolution of body size (or mass) can give rise to hierarchically organized trophic levels with complex between and within trophic interactions. However, because these models have often very different assumptions, sometimes arbitrary, it is difficult to evaluate what are the real key factors that determine food webs evolution, and whether these models' results are robust or not. In this paper, we first review the different adaptive dynamics models, especially highlighting when their assumptions strongly differ. Second, we propose a general model which encompasses all previous models. We show that our model recovers all previous models' results under identical assumptions. However, most importantly, we also show that, when relaxing some of their hypotheses, previous models give rise to degenerate food webs. Third, we show that the assumptions made regarding the form of biomass conversion efficiency are key for food webs evolution, a parameter which was neglected in previous models. We conclude by discussing the implication of biomass conversion efficiency, and by questioning the relevance of such models to study the evolution of food webs

Identifying conversion efficiency as a key mechanism underlying food webs adaptive evolution: a step forward, or backward?

Body size or mass is one of the main factors underlying food webs structure. A large number of evolutionary models have shown that indeed, the adaptive evolution of body size (or mass) can give rise to hierarchically organised trophic levels with complex between and within trophic interactions. However, these models generally make strong arbitrary assumptions on how traits evolve, casting doubts on their robustness. In particular, biomass conversion efficiency is always considered independent of the predator and prey size, which contradicts with the literature. In this paper, we propose a general model encompassing most previous models which allows to show that relaxing arbitrary assumptions gives rise to unrealistic food webs. We then show that considering biomass conversion efficiency dependent on species size is certainly key for food webs adaptive evolution because realistic food webs can evolve, making obsolete the need of arbitrary constraints on traits' evolution. We finally conclude that, on the one hand, ecologists should pay attention to how biomass flows into food webs in models. On the other hand, we question more generally the robustness of evolutionary models for the study of food webs

Identifying conversion efficiency as a key mechanism underlying food webs evolution : a step forward, or backward ?

International audienceBody size or mass is one of the main factors underlying food webs structure. A large number of evolutionary models have shown that indeed, the adaptive evolution of body size (or mass) can give rise to hierarchically organised trophic levels with complex between and within trophic interactions. However, these models generally make strong arbitrary assumptions on how traits evolve, casting doubts on their robustness. In particular, biomass conversion efficiency is always considered independent of the predator and prey size, which contradicts with the literature. In this paper, we propose a general model encompassing most previous models which allows to show that relaxing arbitrary assumptions gives rise to unrealistic food webs. We then show that considering biomass conversion efficiency dependent on species size is certainly key for food webs adaptive evolution because realistic food webs can evolve, making obsolete the need of arbitrary constraints on traits' evolution. We finally conclude that, on the one hand, ecologists should pay attention to how biomass flows into food webs in models. On the other hand, we question more generally the robustness of evolutionary models for the study of food webs

Assessment of hepatocellular carcinoma treatment response with LI-RADS: a pictorial review

Abstract Computed tomography (CT) and magnetic resonance imaging (MRI) play critical roles for assessing treatment response of hepatocellular carcinoma (HCC) after locoregional therapy. Interpretation is challenging because posttreatment imaging findings depend on the type of treatment, magnitude of treatment response, time interval after treatment, and other factors. To help radiologists interpret and report treatment response in a clear, simple, and standardized manner, the Liver Imaging Reporting and Data System (LI-RADS) has developed a Treatment Response (LR-TR) algorithm. Introduced in 2017, the system provides criteria to categorize response of HCC to locoregional treatment (e.g., chemical ablation, energy-based ablation, transcatheter therapy, and radiation therapy). LR-TR categories include Nonevaluable, Nonviable, Equivocal, and Viable. LR-TR does not apply to patients on systemic therapies. This article reviews the LR-TR algorithm; discusses locoregional therapies for HCC, treatment concepts, and expected posttreatment findings; and illustrates LI-RADS treatment response assessment with CT and MRI

Pathogenic T cells have a paradoxical protective effect in murine autoimmune diabetes by boosting Tregs

CD4+CD25+Foxp3+ Tregs play a major role in prevention of autoimmune diseases. The suppressive effect of Tregs on effector T cells (Teffs), the cells that can mediate autoimmunity, has been extensively studied. However, the in vivo impact of Teff activation on Tregs during autoimmunity has not been explored. In this study, we have shown that CD4+ Teff activation strongly boosts the expansion and suppressive activity of Tregs. This helper function of CD4+ T cells, which we believe to be novel, was observed in the pancreas and draining lymph nodes in mouse recipients of islet-specific Teffs and Tregs. Its physiological impact was assessed in autoimmune diabetes. When islet-specific Teffs were transferred alone, they induced diabetes. Paradoxically, when the same Teffs were cotransferred with islet-specific Tregs, they induced disease protection by boosting Treg expansion and suppressive function. RNA microarray analyses suggested that TNF family members were involved in the Teff-mediated Treg boost. In vivo experiments showed that this Treg boost was partially dependent on TNF but not on IL-2. This feedback regulatory loop between Teffs and Tregs may be critical to preventing or limiting the development of autoimmune diseases