Astrin is required for the maintenance of sister chromatid cohesion and centrosome integrity

Faithful chromosome segregation in mitosis requires the formation of a bipolar mitotic spindle with stably attached chromosomes. Once all of the chromosomes are aligned, the connection between the sister chromatids is severed by the cysteine protease separase. Separase also promotes centriole disengagement at the end of mitosis. Temporal coordination of these two activities with the rest of the cell cycle is required for the successful completion of mitosis. In this study, we report that depletion of the microtubule and kinetochore protein astrin results in checkpoint-arrested cells with multipolar spindles and separated sister chromatids, which is consistent with untimely separase activation. Supporting this idea, astrin-depleted cells contain active separase, and separase depletion suppresses the premature sister chromatid separation and centriole disengagement in these cells. We suggest that astrin contributes to the regulatory network that controls separase activity

NOVEL CONCEPTS FOR ISOTOPIC SEPARATION OF 3HE/4HE

The research outlined below established theoretical proof-of-concept using ab initio calculations that {sup 3}He can be separated from {sup 4}He by taking advantage of weak van der Waals interactions with other higher molecular weight rare gases such as xenon. To the best of our knowledge, this is the only suggested method that exploits the physical differences of the isotopes using a chemical interaction

Structural centrosome aberrations promote non-cell-autonomous invasiveness

Centrosomes are the main microtubule-organizing centers of animal cells. Although centrosome aberrations are common in tumors, their consequences remain subject to debate. Here, we studied the impact of structural centrosome aberrations, induced by deregulated expression of ninein-like protein (NLP), on epithelial spheres grown in Matrigel matrices. We demonstrate that NLP-induced structural centrosome aberrations trigger the escape (“budding”) of living cells from epithelia. Remarkably, all cells disseminating into the matrix were undergoing mitosis. This invasive behavior reflects a novel mechanism that depends on the acquisition of two distinct properties. First, NLP-induced centrosome aberrations trigger a re-organization of the cytoskeleton, which stabilizes microtubules and weakens E-cadherin junctions during mitosis. Second, atomic force microscopy reveals that cells harboring these centrosome aberrations display increased stiffness. As a consequence, mitotic cells are pushed out of mosaic epithelia, particularly if they lack centrosome aberrations. We conclude that centrosome aberrations can trigger cell dissemination through a novel, non-cell-autonomous mechanism, raising the prospect that centrosome aberrations contribute to the dissemination of metastatic cells harboring normal centrosomes

Implementing and characterizing precise multi-qubit measurements

There are two general requirements to harness the computational power of quantum mechanics: the ability to manipulate the evolution of an isolated system and the ability to faithfully extract information from it. Quantum error correction and simulation often make a more exacting demand: the ability to perform non-destructive measurements of specific correlations within that system. We realize such measurements by employing a protocol adapted from [S. Nigg and S. M. Girvin, Phys. Rev. Lett. 110, 243604 (2013)], enabling real-time selection of arbitrary register-wide Pauli operators. Our implementation consists of a simple circuit quantum electrodynamics (cQED) module of four highly-coherent 3D transmon qubits, collectively coupled to a high-Q superconducting microwave cavity. As a demonstration, we enact all seven nontrivial subset-parity measurements on our three-qubit register. For each we fully characterize the realized measurement by analyzing the detector (observable operators) via quantum detector tomography and by analyzing the quantum back-action via conditioned process tomography. No single quantity completely encapsulates the performance of a measurement, and standard figures of merit have not yet emerged. Accordingly, we consider several new fidelity measures for both the detector and the complete measurement process. We measure all of these quantities and report high fidelities, indicating that we are measuring the desired quantities precisely and that the measurements are highly non-demolition. We further show that both results are improved significantly by an additional error-heralding measurement. The analyses presented here form a useful basis for the future characterization and validation of quantum measurements, anticipating the demands of emerging quantum technologies.Comment: 10 pages, 5 figures, plus supplemen

Universal Resistances of the Quantum RC circuit

We examine the concept of universal quantized resistance in the AC regime through the fully coherent quantum RC circuit comprising a cavity (dot) capacitively coupled to a gate and connected via a single spin-polarized channel to a reservoir lead. As a result of quantum effects such as the Coulomb interaction in the cavity and global phase coherence, we show that the charge relaxation resistance $R_q$ is identical for weak and large transmissions and it changes from $h/2e^2$ to $h/e^2$ when the frequency (times $\hbar$) exceeds the level spacing of the cavity; $h$ is the Planck constant and $e$ the electron charge. For large cavities, we formulate a correspondence between the charge relaxation resistance $h/e^2$ and the Korringa-Shiba relation of the Kondo model. Furthermore, we introduce a general class of models, for which the charge relaxation resistance is universal. Our results emphasize that the charge relaxation resistance is a key observable to understand the dynamics of strongly correlated systems.Comment: 12 pages, 3 figure

A novel TPR-BEN domain interaction mediates PICH-BEND3 association

PICH is a DNA translocase required for the maintenance of chromosome stability in human cells. Recent data indicate that PICH co-operates with topoisomerase IIα to suppress pathological chromosome missegregation through promoting the resolution of ultra-fine anaphase bridges (UFBs). Here, we identify the BEN domain-containing protein 3 (BEND3) as an interaction partner of PICH in human cells in mitosis. We have purified full length PICH and BEND3 and shown that they exhibit a functional biochemical interaction in vitro. We demonstrate that the PICH-BEND3 interaction occurs via a novel interface between a TPR domain in PICH and a BEN domain in BEND3, and have determined the crystal structure of this TPR-BEN complex at 2.2 Å resolution. Based on the structure, we identified amino acids important for the TPR-BEN domain interaction, and for the functional interaction of the full-length proteins. Our data reveal a proposed new function for BEND3 in association with PICH, and the first example of a specific protein-protein interaction mediated by a BEN domain