Evidence of Raleigh-Hertz surface waves and shear stiffness anomaly in granular media

Due to the non-linearity of Hertzian contacts, the speed of sound in granular matter increases with pressure. Under gravity, the non-linear elastic description predicts that acoustic propagation is only possible through surface modes, called Rayleigh-Hertz modes and guided by the index gradient. Here we directly evidence these modes in a controlled laboratory experiment and use them to probe the elastic properties of a granular packing under vanishing confining pressure. The shape and the dispersion relation of both transverse and sagittal modes are compared to the prediction of non-linear elasticity that includes finite size effects. This allows to test the existence of a shear stiffness anomaly close to the jamming transition.Comment: 4 pages 4 figure

Constrained Cost-Coupled Stochastic Games with Independent State Processes

We consider a non-cooperative constrained stochastic games with N players with the following special structure. With each player there is an associated controlled Markov chain. The transition probabilities of the i-th Markov chain depend only on the state and actions of controller i. The information structure that we consider is such that each player knows the state of its own MDP and its own actions. It does not know the states of, and the actions taken by other players. Finally, each player wishes to minimize a time-average cost function, and has constraints over other time-avrage cost functions. Both the cost that is minimized as well as those defining the constraints depend on the state and actions of all players. We study in this paper the existence of a Nash equilirium. Examples in power control in wireless communications are given.Comment: 7 pages, submitted in september 2006 to Operations Research Letter

Einstein-Weyl structures and Bianchi metrics

We analyse in a systematic way the (non-)compact four dimensional Einstein-Weyl spaces equipped with a Bianchi metric. We show that Einstein-Weyl structures with a Class A Bianchi metric have a conformal scalar curvature of constant sign on the manifold. Moreover, we prove that most of them are conformally Einstein or conformally K\"ahler ; in the non-exact Einstein-Weyl case with a Bianchi metric of the type $VII_0, VIII$ or $IX$, we show that the distance may be taken in a diagonal form and we obtain its explicit 4-parameters expression. This extends our previous analysis, limited to the diagonal, K\"ahler Bianchi $IX$ case.Comment: Latex file, 12 pages, a minor modification, accepted for publication in Class. Quant. Gra

Lattice energy-momentum tensor with Symanzik improved actions

We define the energy-momentum tensor on lattice for the $\lambda \phi^4$ and for the nonlinear $\sigma$-model Symanzik tree-improved actions, using Ward identities or an explicit matching procedure. The resulting operators give the correct one loop scale anomaly, and in the case of the sigma model they can have applications in Monte Carlo simulations.Comment: Self extracting archive fil

Phospho-dependent and phospho-independent interactions of the helicase UPF1 with the NMD factors SMG5-SMG7 and SMG6

Nonsense-mediated mRNA decay (NMD) is a eukaryotic surveillance pathway that recognizes mRNAs with premature stop codons and targets them for rapid degradation. Evidence from previous studies has converged on UPF1 as the central NMD factor. In human cells, the SMG1 kinase phosphorylates UPF1 at the N-terminal and C-terminal tails, in turn allowing the recruitment of the NMD factors SMG5, SMG6 and SMG7. To understand the molecular mechanisms, we recapitulated these steps of NMD in vitro using purified components. We find that a short C-terminal segment of phosphorylated UPF1 containing the last two Ser-Gln motifs is recognized by the heterodimer of SMG5 and SMG7 14-3-3-like proteins. In contrast, the SMG6 14-3-3-like domain is a monomer. The crystal structure indicates that the phosphoserine binding site of the SMG6 14-3-3-like domain is similar to that of SMG5 and can mediate a weak phospho-dependent interaction with UPF1. The dominant SMG6-UPF1 interaction is mediated by a low-complexity region bordering the 14-3-3-like domain of SMG6 and by the helicase domain and C-terminal tail of UPF1. This interaction is phosphorylation independent. Our study demonstrates that SMG5-SMG7 and SMG6 exhibit different and non-overlapping modes of UPF1 recognition, thus pointing at distinguished roles in integrating the complex NMD interaction network

A snapshot of some pLI score pitfalls

The pLI score reflects the tolerance of a given gene to the loss of function on the basis of the number of protein truncating variants, that is, the frameshift, splice donor, splice acceptor, and stop-gain variants referenced for this gene in control databases weighted by the size of the gene and the sequencing coverage. It is frequently used to prioritize candidate genes when analyzing whole exome or whole genome data. We list here the main pitfalls to consider before using this score. Concrete illustrations are given for each of these pitfalls

Cryo-EM reconstructions of inhibitor-bound SMG1 kinase reveal an autoinhibitory state dependent on SMG8

The PI3K-related kinase (PIKK) SMG1 monitors the progression of metazoan nonsense-mediated mRNA decay (NMD) by phosphorylating the RNA helicase UPF1. Previous work has shown that the activity of SMG1 is impaired by small molecule inhibitors, is reduced by the SMG1 interactors SMG8 and SMG9, and is downregulated by the so-called SMG1 insertion domain. However, the molecular basis for this complex regulatory network has remained elusive. Here, we present cryo-electron microscopy reconstructions of human SMG1-9 and SMG1-8-9 complexes bound to either a SMG1 inhibitor or a non-hydrolyzable ATP analog at overall resolutions ranging from 2.8 to 3.6 angstrom. These structures reveal the basis with which a small molecule inhibitor preferentially targets SMG1 over other PIKKs. By comparison with our previously reported substrate-bound structure (Langer et al.,2020), we show that the SMG1 insertion domain can exert an autoinhibitory function by directly blocking the substrate-binding path as well as overall access to the SMG1 kinase active site. Together with biochemical analysis, our data indicate that SMG1 autoinhibition is stabilized by the presence of SMG8. Our results explain the specific inhibition of SMG1 by an ATP-competitive small molecule, provide insights into regulation of its kinase activity within the NMD pathway, and expand the understanding of PIKK regulatory mechanisms in general.Acknowledgements: Daniel Bollschweiler and Tillman Schäfer at the MPIB cryo-EM facility for help with EM data collection and Barbara Steigenberger and Elisabeth Weyher at MPIB biochemistry core facility for carrying out mass spectrometry