Le profil socio-démographique et les activités des médiateurs de CSTI

Cette contribution présente les principaux résultats et les premières analyses d’une enquête quantitative menée dans le cadre de l’École de la médiation : une probable féminisation accrue de la fonction de médiateur dans les prochaines années, une diversité des pratiques et une absence d’unicité dans la dénomination de la fonction contribuant à un manque de reconnaissance du métier

Plant polycistronic precursors containing non-homologous microRNAs target transcripts encoding functionally related proteins

Functional homologous and non-homologous clusters of MIR genes that co-regulate target mRNA transcripts have been identified in plant

MAP Kinase-Mediated Negative Regulation of Symbiotic Nodule Formation in Medicago truncatula

Mitogen-activated protein kinase (MAPK) signaling cascades play critical roles in various cellular events in plants, including stress responses, innate immunity, hormone signaling, and cell specificity. MAPK-mediated stress signaling is also known to negatively regulate nitrogen-fixing symbiotic interactions, but the molecular mechanism of the MAPK signaling cas-cades underlying the symbiotic nodule development remains largely unknown. We show that the MtMKK5-MtMPK3/6 signaling module negatively regulates the early symbiotic nodule formation, probably upstream of ERN1 (ERF Required for Nodulation 1) and NSP1 (Nod factor Signaling Pathway 1) in Medicago truncatula. The overexpression of MtMKK5 stimulated stress and defense signaling pathways but also reduced nodule formation in M. truncatula roots. Conversely, a MAPK specific inhibitor, U0126, enhanced nodule formation and the expression of an early nodulation marker gene, MtNIN. We found that MtMKK5 directly activates MtMPK3/6 by phosphorylating the TEY motif within the activation loop and that the MtMPK3/6 proteins physically interact with the early nodulation-related transcription factors ERN1 and NSP1. These data suggest that the stress signaling-mediated MtMKK5/MtMPK3/6 module sup-presses symbiotic nodule development via the action of early nodulation transcription factors.115Ysciescopuskc

CCL2 modulates cytokine production in cultured mouse astrocytes

<p>Abstract</p> <p>Background</p> <p>The chemokine CCL2 (also known as monocyte chemoattractant protein-1, or MCP-1) is upregulated in patients and rodent models of traumatic brain injury (TBI), contributing to post-traumatic neuroinflammation and degeneration by directing the infiltration of blood-derived macrophages into the injured brain. Our laboratory has previously reported that <it>Ccl2</it>-/- mice show reduced macrophage accumulation and tissue damage, corresponding to improved motor recovery, following experimental TBI. Surprisingly, <it>Ccl2</it>-deficient mice also exhibited delayed but exacerbated secretion of key proinflammatory cytokines in the injured cortex. Thus we sought to further characterise CCL2's potential ability to modulate immunoactivation of astrocytes <it>in vitro</it>.</p> <p>Methods</p> <p>Primary astrocytes were isolated from neonatal wild-type and <it>Ccl2</it>-deficient mice. Established astrocyte cultures were stimulated with various concentrations of lipopolysaccharide (LPS) and interleukin (IL)-1β for up to 24 hours. Separate experiments involved pre-incubation with mouse recombinant (r)CCL2 prior to IL-1β stimulation in wild-type cells. Following stimulation, cytokine secretion was measured in culture supernatant by immunoassays, whilst cytokine gene expression was quantified by real-time reverse transcriptase polymerase chain reaction.</p> <p>Results</p> <p>LPS (0.1-100 μg/ml; 8 h) induced the significantly greater secretion of five key cytokines and chemokines in <it>Ccl2</it>-/- astrocytes compared to wild-type cells. Consistently, IL-6 mRNA levels were 2-fold higher in <it>Ccl2</it>-deficient cells. IL-1β (10 and 50 ng/ml; 2-24 h) also resulted in exacerbated IL-6 production from <it>Ccl2</it>-/- cultures. Despite this, treatment of wild-type cultures with rCCL2 alone (50-500 ng/ml) did not induce cytokine/chemokine production by astrocytes. However, pre-incubation of wild-type astrocytes with rCCL2 (250 ng/ml, 12 h) prior to stimulation with IL-1β (10 ng/ml, 8 h) significantly reduced IL-6 protein and gene expression.</p> <p>Conclusions</p> <p>Our data indicate that astrocytes are likely responsible for the exacerbated cytokine response seen <it>in vivo </it>post-injury in the absence of CCL2. Furthermore, evidence that CCL2 inhibits cytokine production by astrocytes following IL-1β stimulation, suggests a novel, immunomodulatory role for this chemokine in acute neuroinflammation. Further investigation is required to determine the physiological relevance of this phenomenon, which may have implications for therapeutics targeting CCL2-mediated leukocyte infiltration following TBI.</p

Transfer RNA Recognition by Class I Lysyl-tRNA Synthetase from the Lyme Disease Pathogen Borrelia burgdorferi

Borrelia burgdorferi and other spirochetes contain a class I lysyl‐tRNA synthetase (LysRS), in contrast to most eubacteria that have a canonical class II LysRS. We analyzed tRNALys recognition by B. burgdorferi LysRS, using two complementary approaches. First, the nucleotides of B. burgdorferi tRNALys in contact with B. burgdorferi LysRS were determined by enzymatic footprinting experiments. Second, the kinetic parameters for a series of variants of the B. burgdorferi tRNALys were then determined during aminoacylation by B. burgdorferi LysRS. The identity elements were found to be mostly located in the anticodon and in the acceptor stem. Transplantation of the identified identity elements into the Escherichia coli tRNAAsp scaffold endowed lysylation activity on the resulting chimera, indicating that a functional B. burgdorferi lysine tRNA identity set had been determined

Point spread function modelling for astronomical telescopes: a review focused on weak gravitational lensing studies

The accurate modelling of the Point Spread Function (PSF) is of paramount importance in astronomical observations, as it allows for the correction of distortions and blurring caused by the telescope and atmosphere. PSF modelling is crucial for accurately measuring celestial objects' properties. The last decades brought us a steady increase in the power and complexity of astronomical telescopes and instruments. Upcoming galaxy surveys like Euclid and LSST will observe an unprecedented amount and quality of data. Modelling the PSF for these new facilities and surveys requires novel modelling techniques that can cope with the ever-tightening error requirements. The purpose of this review is three-fold. First, we introduce the optical background required for a more physically-motivated PSF modelling and propose an observational model that can be reused for future developments. Second, we provide an overview of the different physical contributors of the PSF, including the optic- and detector-level contributors and the atmosphere. We expect that the overview will help better understand the modelled effects. Third, we discuss the different methods for PSF modelling from the parametric and non-parametric families for ground- and space-based telescopes, with their advantages and limitations. Validation methods for PSF models are then addressed, with several metrics related to weak lensing studies discussed in detail. Finally, we explore current challenges and future directions in PSF modelling for astronomical telescopes.Comment: 63 pages, 14 figures. Submitte

Rethinking data-driven point spread function modeling with a differentiable optical model

In astronomy, upcoming space telescopes with wide-field optical instruments have a spatially varying point spread function (PSF). Specific scientific goals require a high-fidelity estimation of the PSF at target positions where no direct measurement of the PSF is provided. Even though observations of the PSF are available at some positions of the field of view (FOV), they are undersampled, noisy, and integrated into wavelength in the instrument's passband. PSF modeling represents a challenging ill-posed problem, as it requires building a model from degraded observations that can infer a super-resolved PSF at any wavelength and position in the FOV. Our model, coined WaveDiff, proposes a paradigm shift in the data-driven modeling of the point spread function field of telescopes. We change the data-driven modeling space from the pixels to the wavefront by adding a differentiable optical forward model into the modeling framework. This change allows the transfer of complexity from the instrumental response into the forward model. The proposed model relies on stochastic gradient descent to estimate its parameters. Our framework paves the way to building powerful, physically motivated models that do not require special calibration data. This paper demonstrates the WaveDiff model in a simplified setting of a space telescope. The proposed framework represents a performance breakthrough with respect to the existing state-of-the-art data-driven approach. The pixel reconstruction errors decrease 6-fold at observation resolution and 44-fold for a 3x super-resolution. The ellipticity errors are reduced at least 20 times, and the size error is reduced more than 250 times. By only using noisy broad-band in-focus observations, we successfully capture the PSF chromatic variations due to diffraction. Code available at https://github.com/tobias-liaudat/wf-psf.Comment: Submitted. Without appendix: 42 pages, 10 figures, 4 table