Relaxation volumes of microscopic and mesoscopic irradiation-induced defects in tungsten

The low-energy structures of irradiation-induced defects in materials have been studied extensively over several decades, as these determine the available modes by which a defect can diffuse or relax, and how the microstructure of an irradiated material evolves as a function of temperature and time. Consequently, many studies concern the relative energies of possible defect structures, and empirical potentials are commonly fitted to or evaluated with respect to these. But recently [S. L. Dudarev et al., Nucl. Fusion 58, 126002 (2018)], we have shown that other parameters of defects not directly related to defect energies, namely, their elastic dipole tensors and relaxation volumes, determine the stresses, strains, and swelling of reactor components under irradiation. These elastic properties of defects have received comparatively little attention. In this study, we compute relaxation volumes of irradiation-induced defects in tungsten using empirical potentials and compare to density functional theory results. Different empirical potentials give different results, but some clear potential-independent trends can be identified. We show that the relaxation volume of a small defect cluster can be predicted to within 10% from its point-defect count. For larger defect clusters, we provide empirical fits as a function of defect cluster size. We demonstrate that the relaxation volume associated with a single primary-damage cascade can be estimated from the primary knock-on atom energy. We conclude that while annihilation of defects invariably reduces the total relaxation volume of the cascade debris, there is still no conclusive verdict about whether coalescence of defects reduces or increases the total relaxation volume. Published under license by AIP Publishing.Peer reviewe

Requirements for F-BAR Proteins TOCA-1 and TOCA-2 in Actin Dynamics and Membrane Trafficking during Caenorhabditis elegans Oocyte Growth and Embryonic Epidermal Morphogenesis

The TOCA family of F-BAR–containing proteins bind to and remodel lipid bilayers via their conserved F-BAR domains, and regulate actin dynamics via their N-Wasp binding SH3 domains. Thus, these proteins are predicted to play a pivotal role in coordinating membrane traffic with actin dynamics during cell migration and tissue morphogenesis. By combining genetic analysis in Caenorhabditis elegans with cellular biochemical experiments in mammalian cells, we showed that: i) loss of CeTOCA proteins reduced the efficiency of Clathrin-mediated endocytosis (CME) in oocytes. Genetic interference with CeTOCAs interacting proteins WSP-1 and WVE-1, and other components of the WVE-1 complex, produced a similar effect. Oocyte endocytosis defects correlated well with reduced egg production in these mutants. ii) CeTOCA proteins localize to cell–cell junctions and are required for proper embryonic morphogenesis, to position hypodermal cells and to organize junctional actin and the junction-associated protein AJM-1. iii) Double mutant analysis indicated that the toca genes act in the same pathway as the nematode homologue of N-WASP/WASP, wsp-1. Furthermore, mammalian TOCA-1 and C. elegans CeTOCAs physically associated with N-WASP and WSP-1 directly, or WAVE2 indirectly via ABI-1. Thus, we propose that TOCA proteins control tissues morphogenesis by coordinating Clathrin-dependent membrane trafficking with WAVE and N-WASP–dependent actin-dynamics

Transport polarisé de l'E-Cadhérine dans des cellules épithéliales de la drosophile

Le réseau des jonctions reliant les cellules entre-elles, les jonctions adhérentes (AJ), est nécessaire pour la fonction et la morphologie de l épithélium. La stabilité et plasticité des AJ repose sur l exocytose et l endocytose de la protéine E-Cadhérine (E-Cad). Ma thèse montre que la perte de fonction des protéines Cdc42, Par-6 ou aPKC s accompagne d une accumulation apicale de structures intracellulaires d E-Cad et d une perturbation des AJ dans les cellules épithéliales de drosophile. Les structures ponctuelles proviennent de vésicules élargies et malformées qui émanent des AJ. Nous montrons que la protéine Cip4 est un effecteur de Cdc42 qui interagit avec la Dynamine et WASp (activateur d Arp2/3). En conséquence, la perte de fonction des protéines Cip4, WASp ou Arp2/3 aboutit également à un défaut de l endocytose de l E-Cad. Cip4 et WASp agissent donc comme un lien entre Cdc42/Par-6/aPKC et le mécanisme d endocytose précoce pour réguler l endocytose de l E-Cad dans l épithéliumPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Transcriptional control of a plant stem cell niche

Despite the independent evolution of multicellularity in plants and animals, the basic organization of their stem cell niches is remarkably similar. Here, we report the genome-wide regulatory potential of WUSCHEL, the key transcription factor for stem cell maintenance in the shoot apical meristem of the reference plant Arabidopsis thaliana. WUSCHEL acts by directly binding to at least two distinct DNA motifs in more than 100 target promoters and preferentially affects the expression of genes with roles in hormone signaling, metabolism, and development. Striking examples are the direct transcriptional repression of CLAVATA1, which is part of a negative feedback regulation of WUSCHEL, and the immediate regulation of transcriptional repressors of the TOPLESS family, which are involved in auxin signaling. Our results shed light on the complex transcriptional programs required for the maintenance of a dynamic and essential stem cell niche.Fil: Busch, Wolfang. Max Planck Institute For Developmental Biology; Alemania. University of Duke; Estados UnidosFil: Miotk, Andrej. University of Heidelberg; AlemaniaFil: Ariel, Federico Damian. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Agrobiotecnología del Litoral. Universidad Nacional del Litoral. Instituto de Agrobiotecnología del Litoral; ArgentinaFil: Zhao, Zhong. University of Heidelberg; AlemaniaFil: Forner, Joachim. University of Heidelberg; AlemaniaFil: Daum, Gabor. University of Heidelberg; AlemaniaFil: Suzaki, Takuya. University of Heidelberg; AlemaniaFil: Schuster, Christoph. University of Heidelberg; AlemaniaFil: Schultheiss, Sebastian J.. Max Planck Institute For Developmental Biology; AlemaniaFil: Leibfried, Andrea. Max Planck Institute For Developmental Biology; AlemaniaFil: Haubeiß, Silke. Max Planck Institute For Developmental Biology; AlemaniaFil: Ha, Nati. University of Heidelberg; AlemaniaFil: Chan, Raquel Lia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe. Instituto de Agrobiotecnología del Litoral. Universidad Nacional del Litoral. Instituto de Agrobiotecnología del Litoral; ArgentinaFil: Lohmann, Jan U.. Max Planck Institute For Developmental Biology; Alemania. University of Heidelberg; Alemani