Aix-Marseille University

About: Aix-Marseille University is a education organization based out in Marseille, France. It is known for research contribution in the topics: Population & Galaxy. The organization has 24326 authors who have published 54240 publications receiving 1455416 citations. The organization is also known as: University Aix-Marseille & université d'Aix-Marseille.

Planck 2015 results. XXII. A map of the thermal Sunyaev-Zeldovich effect

Abstract: We have constructed all-sky Compton parameters maps, y-maps, of the thermal Sunyaev-Zeldovich (tSZ) effect by applying specifically tailored component separation algorithms to the 30 to 857 GHz frequency channel maps from the Planck satellite These reconstructed y-maps are delivered as part of the Planck 2015 release The y-maps are characterized in terms of noise properties and residual foreground contamination, mainly thermal dust emission at large angular scales, and cosmic infrared background and extragalactic point sources at small angular scales Specific masks are defined to minimize foreground residuals and systematics Using these masks, we compute the y-map angular power spectrum and higher order statistics From these we conclude that the y-map is dominated by tSZ signal in the multipole range, 20

Search for new phenomena in the dijet mass distribution using pp collision data at √s = 8 TeV with the ATLAS detector

Abstract: Dijet events produced in LHC proton-proton collisions at a center-of-mass energy s√=8 TeV are studied with the ATLAS detector using the full 2012 data set, with an integrated luminosity of 20.3 f ...

A self-organized biomechanical network drives shape changes during tissue morphogenesis

Abstract: Feedbacks between the dissociation and advection of myosin II result in self-organized behaviour of actomyosin networks that drives shape changes during tissue morphogenesis. Cell–cell intercalation during tissue elongation is orchestrated by actomyosin networks in which pulses of assembly and disassembly induce shape deformations that can be stabilized by a localized pool of actomyosin. What controls these mechanical ratchets has been unclear. Here Thomas Lecuit and colleagues present a potentially general model in which feedbacks between dissociation and advection of myosin II components set the frequency and amplitude of these pulses. Thus, the self-organizing properties of the actomyosin network are sufficient to define the cell shape changes that govern cell intercalation during morphogenesis. Tissue morphogenesis is orchestrated by cell shape changes. Forces required to power these changes are generated by non-muscle myosin II (MyoII) motor proteins pulling filamentous actin (F-actin). Actomyosin networks undergo cycles of assembly and disassembly (pulses)1,2 to cause cell deformations alternating with steps of stabilization to result in irreversible shape changes3,4,5,6. Although this ratchet-like behaviour operates in a variety of contexts, the underlying mechanisms remain unclear. Here we investigate the role of MyoII regulation through the conserved Rho1–Rok pathway7 during Drosophila melanogaster germband extension. This morphogenetic process is powered by cell intercalation, which involves the shrinkage of junctions in the dorsal–ventral axis (vertical junctions) followed by junction extension in the anterior–posterior axis8. While polarized flows of medial–apical MyoII pulses deform vertical junctions, MyoII enrichment on these junctions (planar polarity) stabilizes them6. We identify two critical properties of MyoII dynamics that underlie stability and pulsatility: exchange kinetics governed by phosphorylation–dephosphorylation cycles of the MyoII regulatory light chain; and advection due to contraction of the motors on F-actin networks. Spatial control over MyoII exchange kinetics establishes two stable regimes of high and low dissociation rates, resulting in MyoII planar polarity. Pulsatility emerges at intermediate dissociation rates, enabling convergent advection of MyoII and its upstream regulators Rho1 GTP, Rok and MyoII phosphatase. Notably, pulsatility is not an outcome of an upstream Rho1 pacemaker. Rather, it is a self-organized system that involves positive and negative biomechanical feedback between MyoII advection and dissociation rates.