31 research outputs found

    Combination of searches for heavy spin-1 resonances using 139 fb−1 of proton-proton collision data at s = 13 TeV with the ATLAS detector

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    A combination of searches for new heavy spin-1 resonances decaying into different pairings of W, Z, or Higgs bosons, as well as directly into leptons or quarks, is presented. The data sample used corresponds to 139 fb−1 of proton-proton collisions at = 13 TeV collected during 2015–2018 with the ATLAS detector at the CERN Large Hadron Collider. Analyses selecting quark pairs (qq, bb, , and tb) or third-generation leptons (τν and ττ) are included in this kind of combination for the first time. A simplified model predicting a spin-1 heavy vector-boson triplet is used. Cross-section limits are set at the 95% confidence level and are compared with predictions for the benchmark model. These limits are also expressed in terms of constraints on couplings of the heavy vector-boson triplet to quarks, leptons, and the Higgs boson. The complementarity of the various analyses increases the sensitivity to new physics, and the resulting constraints are stronger than those from any individual analysis considered. The data exclude a heavy vector-boson triplet with mass below 5.8 TeV in a weakly coupled scenario, below 4.4 TeV in a strongly coupled scenario, and up to 1.5 TeV in the case of production via vector-boson fusion

    The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis

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    In budding yeast, a signaling network known as the mitotic exit network (MEN) triggers exit from mitosis. We find that hypertonic stress allows MEN mutants to exit from mitosis in a manner dependent on the high osmolarity glycerol (HOG) mitogen-activated protein (MAP) kinase cascade. The HOG pathway drives exit from mitosis in MEN mutants by promoting the activation of the MEN effector, the protein phosphatase Cdc14. Activation of Cdc14 depends on the Cdc14 early anaphase release network, a group of proteins that functions in parallel to the MEN to promote Cdc14 function. Notably, exit from mitosis is promoted by the signaling branch defined by the Sho1 osmosensing system, but not by the Sln1 osmosensor of the HOG pathway. Our results suggest that the stress MAP kinase pathway mobilizes programs to promote completion of the cell cycle and entry into G(1) under unfavorable conditions

    Functional characterization of lysosomal interaction of Akt with VRK2

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    Serine-threonine kinase Akt (also known as PKB, protein kinase B), a core intracellular mediator of cell survival, is involved in various human cancers and has been suggested to play an important role in the regulation of autophagy in mammalian cells. Nonetheless, the physiological function of Akt in the lysosomes is currently unknown. We have reported previously that PtdIns (3)P-dependent lysosomal accumulation of the Akt-Phafin2 complex is a critical step for autophagy induction. Here, to characterize the molecular function of activated Akt in the lysosomes in the process of autophagy, we searched for the molecules that interact with the Akt complex at the lysosomes after induction of autophagy. By time-of-flight-mass spectrometry (TOF/MS) analysis, kinases of the VRK family, a unique serine-threonine family of kinases in the human kinome, were identified. VRK2 interacts with Akt1 and Akt2, but not with Akt3; the C terminus of Akt and the N terminus of VRK2 facilitate the interaction of Akt and VRK2 in mammalian cells. The kinase-dead form of VRK2A (KD VRK2A) failed to interact with Akt in coimmunoprecipitation assays. Bimolecular fluorescence complementation (BiFC) experiments showed that, in the lysosomes, Akt interacted with VRK2A but not with VRK2B or KD VRK2A. Immunofluorescent assays revealed that VRK2 and phosphorylated Akt accumulated in the lysosomes after autophagy induction. WT VRK2A, but not KD VRK2A or VRK2B, facilitated accumulation of phosphorylated Akt in the lysosomes. Downregulation of VRK2 abrogated the lysosomal accumulation of phosphorylated Akt and impaired nuclear localization of TFEB; these events coincided to inhibition of autophagy induction. The VRK2-Akt complex is required for control of lysosomal size, acidification, bacterial degradation, and for viral replication. Moreover, lysosomal VRK2-Akt controls cellular proliferation and mitochondria) outer-membrane stabilization. Given the roles of autophagy in the pathogenesis of human cancer, the current study provides a novel insight into the oncogenic activity of VRK2-Akt complexes in the lysosomes via modulation of autophagy

    The Multiple Roles of Cohesin in Meiotic Chromosome Morphogenesis and Pairing

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    Sister chromatid cohesion, mediated by cohesin complexes, is laid down during DNA replication and is essential for the accurate segregation of chromosomes. Previous studies indicated that, in addition to their cohesion function, cohesins are essential for completion of recombination, pairing, meiotic chromosome axis formation, and assembly of the synaptonemal complex (SC). Using mutants in the cohesin subunit Rec8, in which phosphorylated residues were mutated to alanines, we show that cohesin phosphorylation is not only important for cohesin removal, but that cohesin's meiotic prophase functions are distinct from each other. We find pairing and SC formation to be dependent on Rec8, but independent of the presence of a sister chromatid and hence sister chromatid cohesion. We identified mutations in REC8 that differentially affect Rec8's cohesion, pairing, recombination, chromosome axis and SC assembly function. These findings define Rec8 as a key determinant of meiotic chromosome morphogenesis and a central player in multiple meiotic events.United States National Institutes of Health (Grant GM62207)National Science Foundatio

    Measurement of vector boson production cross sections and their ratios using pp collisions at <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" altimg="si1.svg"><mml:msqrt><mml:mrow><mml:mi>s</mml:mi></mml:mrow></mml:msqrt><mml:mo linebreak="goodbreak" linebreakstyle="after">=</mml:mo><mml:mn>13.6</mml:mn></mml:math> TeV with the ATLAS detector

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    Fiducial and total W± and Z boson cross sections, their ratios and the ratio of top-antitop-quark pair and W-boson fiducial cross sections are measured in proton–proton collisions at a centre-of-mass energy of s=13.6 TeV, corresponding to an integrated luminosity of 29 fb−1 of data collected in 2022 by the ATLAS experiment at the Large Hadron Collider. The measured fiducial cross-section values for W+→ℓ+ν, W−→ℓ−ν¯, and Z→ℓ+ℓ− (ℓ=e or μ) boson productions are 4250±150 pb, 3310±120 pb, and 744±20 pb, respectively, where the uncertainty is the total uncertainty, including that arising from the luminosity of about 2.2%. The measurements are in agreement with Standard-Model predictions calculated at next-to-next-to-leading-order in αs, next-to-next-to-leading logarithmic accuracy and next-to-leading-order electroweak accuracy

    Search for heavy neutral Higgs bosons decaying into a top quark pair in 140 fb−1 of proton-proton collision data at s \sqrt{s} = 13 TeV with the ATLAS detector

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    Abstract A search for heavy pseudo-scalar (A) and scalar (H) Higgs bosons decaying into a top-quark pair (tt t\overline{t} t t ¯ ) has been performed with 140 fb−1 of proton-proton collision data collected by the ATLAS experiment at the Large Hadron Collider at a centre-of-mass energy of s \sqrt{s} s = 13 TeV. Interference effects between the signal process and Standard Model (SM) tt t\overline{t} t t ¯ production are taken into account. Final states with exactly one or exactly two electrons or muons are considered. No significant deviation from the SM prediction is observed. The results of the search are interpreted in the context of a two-Higgs-doublet model (2HDM) of type II in the alignment limit with mass-degenerate pseudo-scalar and scalar Higgs bosons (mA = mH) and the hMSSM parameterisation of the minimal supersymmetric extension of the Standard Model. Ratios of the two vacuum expectation values, tan β, smaller than 3.49 (3.16) are excluded at 95% confidence level for mA = mH = 400 GeV in the 2HDM (hMSSM). Masses up to 1240 GeV are excluded for the lowest tested tan β value of 0.4 in the 2HDM. In the hMSSM, masses up to 950 GeV are excluded for tan β = 1.0. In addition, generic exclusion limits are derived separately for single scalar and pseudo-scalar states for different choices of their mass and total width.</jats:p
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