The Drosophila fragile X-related gene regulates axoneme differentiation during spermatogenesis

AbstractMacroorchidism (i.e., enlarged testicles) and mental retardation are the two hallmark symptoms of Fragile X syndrome (FraX). The disease is caused by loss of fragile X mental retardation protein (FMRP), an RNA-binding translational regulator. We previously established a FraX model in Drosophila, showing that the fly FMRP homologue, dFXR, acts as a negative translational regulator of microtubule-associated Futsch to control stability of the microtubule cytoskeleton during nervous system development. Here, we investigate dFXR function in the testes. Male dfxr null mutants have the enlarged testes characteristic of the disease and are nearly sterile (>90% reduced male fecundity). dFXR protein is highly enriched in Drosophila testes, particularly in spermatogenic cells during the early stages of spermatogenesis. Cytological analyses reveal that spermatogenesis is arrested specifically in late-stage spermatid differentiation following individualization. Ultrastructurally, dfxr mutants lose specifically the central pair microtubules in the sperm tail axoneme. The frequency of central pair microtubule loss becomes progressively greater as spermatogenesis progresses, suggesting that dFXR regulates microtubule stability. Proteomic analyses reveal that chaperones Hsp60B-, Hsp68-, Hsp90-related protein TRAP1, and other proteins have altered expression in dfxr mutant testes. Taken together with our previous nervous system results, these data suggest a common model in which dFXR regulates microtubule stability in both synaptogenesis in the nervous system and spermatogenesis in the testes. The characterization of dfxr function in the testes paves the way to genetic screens for modifiers of dfxr-induced male sterility, as a means to efficiently dissect FMRP-mediated mechanisms

Comparison of models for the simulation of landslide generated Tsunamis

In this paper, we analyze the relevance of the use of the shallow water model and the Boussinesq model to simulate tsunamis generated by a landslide. In a first part, we determine if the two models are able to reproduce waves generated by a landslide. Each model has drawbacks but it seems that it is possible to use them together to improve the simulations. In a second part we try to recover the landslide displacement from the generated wave. This problem is formulated as a minimization problem and we limit the number of parameters to determine assuming that the bottom can be well described by an empirical law

Initial-State Interactions in the Unpolarized Drell-Yan Process

We show that initial-state interactions contribute to the $\cos 2 \phi$ distribution in unpolarized Drell-Yan lepton pair production $p p$ and $p \bar p \to \ell^+ \ell^- X$, without suppression. The asymmetry is expressed as a product of chiral-odd distributions $h_1^\perp(x_1,\bm{p}_\perp^2)\times \bar h_1^\perp(x_2,\bm{k}_\perp^2)$, where the quark-transversity function $h_1^\perp(x,\bm{p}_\perp^2)$ is the transverse momentum dependent, light-cone momentum distribution of transversely polarized quarks in an {\it unpolarized} proton. We compute this (naive) $T$-odd and chiral-odd distribution function and the resulting $\cos 2 \phi$ asymmetry explicitly in a quark-scalar diquark model for the proton with initial-state gluon interaction. In this model the function $h_1^\perp(x,\bm{p}_\perp^2)$ equals the $T$-odd (chiral-even) Sivers effect function $f^\perp_{1T}(x,\bm{p}_\perp^2)$. This suggests that the single-spin asymmetries in the SIDIS and the Drell-Yan process are closely related to the $\cos 2 \phi$ asymmetry of the unpolarized Drell-Yan process, since all can arise from the same underlying mechanism. This provides new insight regarding the role of quark and gluon orbital angular momentum as well as that of initial- and final-state gluon exchange interactions in hard QCD processes.Comment: 22 pages, 6 figure

Разработка ингибиторов коррозии сталей на основе тиомочевины и наночастиц металлов

Despite the essential role of the fibrinogen gamma-chain as a blood clotting factor, the fibrinogen gamma-chain contains a number of interaction sites to recruit other factors such as leukocytes important for prevention of pathogen entry and propagation of the repair process. Interleukin-6 (IL-6) is known as the major inducer of gamma-fibrinogen synthesis in hepatocytes, whereas IL-1beta has been shown to act as a potent inhibitor of gamma-fibrinogen expression. Studies on the rat fibrinogen gamma-chain promoter suggest that nuclear factor (NF)-kappaB replaces the signal transducer and activator of transcription (STAT) 3 from binding to overlapping NF-kappaB/STAT3 binding sites within the 5' regulatory region of the rat gamma-chain gene promoter. However, despite its physiological relevance, the underlying mechanism responsible for the inhibitory effect of IL-1beta in humans is still not understood and apparently more complex. In contrast to the mechanism described for the rat gene our results indicate that IL-1beta suppresses the IL-6-induced activation of the human gamma-fibrinogen gene particularly by blocking the late phase STAT3-tyrosine phosphorylation NF-kappaB-dependently but independent from de novo protein synthesis. Consequently, blocking NF-kappaB activation restores specifically late phase STAT3 activation as well as the induction of the human gamma-fibrinogen gene. In contrast, specifically early STAT3 activation could be restored by a block of the p38 mitogen-activated protein kinase (p38(MAPK)) pathway. In summary, our results indicate that expression of the gamma-fibrinogen gene is mainly controlled by the strength of late phase STAT3 activation, which in turn is negatively regulated by the extent of IL-1beta-mediated NF-kappaB activity

Transduction of intracellular and intercellular dynamics in yeast glycolytic oscillations.

AbstractUnder certain well-defined conditions, a population of yeast cells exhibits glycolytic oscillations that synchronize through intercellular acetaldehyde. This implies that the dynamic phenomenon of the oscillation propagates within and between cells. We here develop a method to establish by which route dynamics propagate through a biological reaction network. Application of the method to yeast demonstrates how the oscillations and the synchronization signal can be transduced. That transduction is not so much through the backbone of glycolysis, as via the Gibbs energy and redox coenzyme couples (ATP/ADP, and NADH/NAD), and via both intra- and intercellular acetaldehyde

Azimuthal asymmetries in lepton-pair production at a fixed-target experiment using the LHC beams (AFTER)

A multi-purpose fixed-target experiment using the proton and lead-ion beams of the LHC was recently proposed by Brodsky, Fleuret, Hadjidakis and Lansberg, and here we concentrate our study on some issues related to the spin physics part of this project (referred to as AFTER). We study the nucleon spin structure through $pp$ and $pd$ processes with a fixed-target experiment using the LHC proton beams, for the kinematical region with 7 TeV proton beams at the energy in center-of-mass frame of two nucleons $\sqrt{s}=115$ GeV. We calculate and estimate the $\cos2\phi$ azimuthal asymmetries of unpolarized $pp$ and $pd$ dilepton production processes in the Drell--Yan continuum region and at the $Z$-pole. We also calculate the $\sin(2\phi-\phi_S)$, $\sin(2\phi+\phi_S)$ and $\sin2\phi$ azimuthal asymmetries of $pp$ and $pd$ dilepton production processes with the target proton and deuteron longitudinally or transversally polarized in the Drell--Yan continuum region and around $Z$ resonances region. We conclude that it is feasible to measure these azimuthal asymmetries, consequently the three-dimensional or transverse momentum dependent parton distribution functions (3dPDFs or TMDs), at this new AFTER facility.Comment: 15 pages, 40 figures. Version accepted for publication in EPJ

Angular Distributions of Drell-Yan Lepton Pairs at the Tevatron: Order αs2\alpha_s^2 Corrections and Monte Carlo Studies

We investigate the angular distribution of the lepton pair in the process $p \bar{p} \rightarrow \gamma^{\ast} + X \rightarrow \ell^+\ell^- + X$, where the virtual photon is produced at high transverse momentum. The angular distribution of the leptons is very sensitive to possible nonperturbative effects, such as a nontrivial vacuum structure of QCD, and offers a good chance to test such effects. We present complete ${\cal O}(\alpha_s^2)$ calculations of the decay lepton distributions in the lepton pair rest frame. An order ${\cal O}(\alpha_s)$ Monte Carlo study of the lepton angular distributions, with acceptance cuts and energy resolution smearing applied to the leptons, is also presented.Comment: 26 pages (Revtex) plus 9 (uuencoded) postscript figures available as a compressed tar file at ftp://phenom.physics.wisc.edu/pub/preprints/madph-94-857-figs.tar.