1,166 research outputs found
Induced Delocalization by Correlation and Interaction in the one-dimensional Anderson Model
We consider long-range correlated disorder and mutual interacting particles
according to a dipole-dipole coupling as modifications to the one-dimensional
Anderson model. Technically we rely on the (numerical) exact diagonalization of
the system's Hamilitonian. From the perspective of different localization
measures we confirm and extend the picture of the emergence of delocalized
states with increasing correlations. Beside these studies a definition for
multi-particle localization is proposed. In the case of two interacting bosons
we observe a sensitivity of localization with respect to the range of the
particle-particle interaction and insensitivity to the coupling's sign, which
should stimulate new theoretical approaches and experimental investigations
with e.g. dipolar cold quantum gases.
This revised manuscript is much more explicit compared to the initial version
of the paper. Major extensions have been applied to Sects. II and III where we
updated and added figures and we more extensively compared our results to the
literature. Furthermore, Sect. III additionally contains a phenomenological
line of reasoning that bridges from delocalization by correlation to
delocalization by interaction on the basis of the multi-particle Hamilton
matrix
ATM and Artemis promote homologous recombination of radiation-induced DNA double-strand breaks in G2
Homologous recombination (HR) and nonâhomologous end joining (NHEJ) represent distinct pathways for repairing DNA doubleâstrand breaks (DSBs). Previous work implicated Artemis and ATM in an NHEJâdependent process, which repairs a defined subset of radiationâinduced DSBs in G1âphase. Here, we show that in G2, as in G1, NHEJ represents the major DSBârepair pathway whereas HR is only essential for repair of âŒ15% of Xâ or Îłârayâinduced DSBs. In addition to requiring the known HR proteins, Brca2, Rad51 and Rad54, repair of radiationâinduced DSBs by HR in G2 also involves Artemis and ATM suggesting that they promote NHEJ during G1 but HR during G2. The dependency for ATM for repair is relieved by depleting KAPâ1, providing evidence that HR in G2 repairs heterochromatinâassociated DSBs. Although not core HR proteins, ATM and Artemis are required for efficient formation of singleâstranded DNA and Rad51 foci at radiationâinduced DSBs in G2 with Artemis function requiring its endonuclease activity. We suggest that Artemis endonuclease removes lesions or secondary structures, which inhibit end resection and preclude the completion of HR or NHEJ
DNA double-strand breaks in heterochromatin elicit fast repair protein recruitment, histone H2AX phosphorylation and relocation to euchromatin
DNA double-strand breaks (DSBs) can induce chromosomal aberrations and carcinogenesis and their correct repair is crucial for genetic stability. The cellular response to DSBs depends on damage signaling including the phosphorylation of the histone H2AX (ÎłH2AX). However, a lack of ÎłH2AX formation in heterochromatin (HC) is generally observed after DNA damage induction. Here, we examine ÎłH2AX and repair protein foci along linear ion tracks traversing heterochromatic regions in human or murine cells and find the DSBs and damage signal streaks bending around highly compacted DNA. Given the linear particle path, such bending indicates a relocation of damage from the initial induction site to the periphery of HC. Real-time imaging of the repair protein GFP-XRCC1 confirms fast recruitment to heterochromatic lesions inside murine chromocenters. Using single-ion microirradiation to induce localized DSBs directly within chromocenters, we demonstrate that H2AX is early phosphorylated within HC, but the damage site is subsequently expelled from the center to the periphery of chromocenters within âŒ20âmin. While this process can occur in the absence of ATM kinase, the repair of DSBs bordering HC requires the protein. Finally, we describe a local decondensation of HC at the sites of ion hits, potentially allowing for DSB movement via physical forces
Opposing roles for 53BP1 during homologous recombination
Although DNA non-homologous end-joining repairs most DNA double-strand breaks (DSBs) in G2 phase, late repairing DSBs undergo resection and repair by homologous recombination (HR). Based on parallels to the situation in G1 cells, previous work has suggested that DSBs that undergo repair by HR predominantly localize to regions of heterochromatin (HC). By using H3K9me3 and H4K20me3 to identify HC regions, we substantiate and extend previous evidence, suggesting that HC-DSBs undergo repair by HR. Next, we examine roles for 53BP1 and BRCA1 in this process. Previous studies have shown that 53BP1 is pro-non-homologous end-joining and anti-HR. Surprisingly, we demonstrate that in G2 phase, 53BP1 is required for HR at HC-DSBs with its role being to promote phosphorylated KAP-1 foci formation. BRCA1, in contrast, is dispensable for pKAP-1 foci formation but relieves the barrier caused by 53BP1. As 53BP1 is retained at irradiation-induced foci during HR, we propose that BRCA1 promotes displacement but retention of 53BP1 to allow resection and any necessary HC modifications to complete HR. In contrast to this role for 53BP1 in HR in G2 phase, we show that it is dispensable for HR in S phase, where HC regions are likely relaxed during replication
Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1
DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding proteinâinteracting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Kuâ/â mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847
DNA double-strand breaks in heterochromatin elicit fast repair protein recruitment, histone H2AX phosphorylation and relocation to euchromatin
DNA double-strand breaks (DSBs) can induce chromosomal aberrations and carcinogenesis and their correct repair is crucial for genetic stability. The cellular response to DSBs depends on damage signaling including the phosphorylation of the histone H2AX (ÎłH2AX). However, a lack of ÎłH2AX formation in heterochromatin (HC) is generally observed after DNA damage induction. Here, we examine ÎłH2AX and repair protein foci along linear ion tracks traversing heterochromatic regions in human or murine cells and find the DSBs and damage signal streaks bending around highly compacted DNA. Given the linear particle path, such bending indicates a relocation of damage from the initial induction site to the periphery of HC. Real-time imaging of the repair protein GFP-XRCC1 confirms fast recruitment to heterochromatic lesions inside murine chromocenters. Using single-ion microirradiation to induce localized DSBs directly within chromocenters, we demonstrate that H2AX is early phosphorylated within HC, but the damage site is subsequently expelled from the center to the periphery of chromocenters within âŒ20âmin. While this process can occur in the absence of ATM kinase, the repair of DSBs bordering HC requires the protein. Finally, we describe a local decondensation of HC at the sites of ion hits, potentially allowing for DSB movement via physical forces
Umsetzung der Energiestrategie 2050: Herausforderungen und Chancen fĂŒr Staat und Wirtschaft
Sammelband der Reihe "Energy Governance Working Paper" Nr. 1 bis 7Die Energiestrategie 2050 des Bundes definiert anspruchsvolle Ziele. FĂŒr deren Erreichung hat der Bundesrat daher unter anderem den Aktionsplan Energieforschung ins Leben gerufen. Dazu wurden acht sogenannte SCCERs, Swiss Competence Center for Energy Research, initiiert, in denen hochschulĂŒbergreifend angewandte Energie-Forschung betrieben wird. Die ZĂŒrcher Hochschule fĂŒr Angewandte Wissenschaften (ZHAW) ist an vier dieser acht SCCERs aktiv beteiligt.
Die ZHAW hat diese Aufgabe zum Anlass genommen, Energieforschung zum strategischen Schwerpunkt der gesamten Fachhochschule zu erklĂ€ren und in allen Departementen Kompetenzaufbauprojekte zu starten. Der vorliegende Sammelband prĂ€sentiert die ersten Ergebnisse dieser Kompetenzaufbauprojekte an der School of Management and Law, wobei zwei dieser Projekte in Zusammenarbeit mit Forschern aus den Departementen Angewandte Linguistik und School of Engineering erfolgten. Dabei wurden die Herausforderungen und Chancen, die sich fĂŒr Staat und Wirtschaft aus der Umsetzung der Energiestrategie 2050 ableiten, auf verschiedenen Ebenen betrachtet: die Schweiz im internationalen Vergleich, Besonderheiten der FĂŒhrung von EVUs, rechtliche und ökonomische Rahmenbedingungen und die Gestaltung der Energie-Zukunft in Schweizer StĂ€dten
Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1
DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homologous recombination (HR). The C terminal binding proteinâinteracting protein (CtIP) is phosphorylated in G2 by cyclin-dependent kinases to initiate resection and promote HR. CtIP also exerts functions during NHEJ, although the mechanism phosphorylating CtIP in G1 is unknown. In this paper, we identify Plk3 (Polo-like kinase 3) as a novel DSB response factor that phosphorylates CtIP in G1 in a damage-inducible manner and impacts on various cellular processes in G1. First, Plk3 and CtIP enhance the formation of ionizing radiation-induced translocations; second, they promote large-scale genomic deletions from restriction enzyme-induced DSBs; third, they are required for resection and repair of complex DSBs; and finally, they regulate alternative NHEJ processes in Kuâ/â mutants. We show that mutating CtIP at S327 or T847 to nonphosphorylatable alanine phenocopies Plk3 or CtIP loss. Plk3 binds to CtIP phosphorylated at S327 via its Polo box domains, which is necessary for robust damage-induced CtIP phosphorylation at S327 and subsequent CtIP phosphorylation at T847
The Long-Baseline Neutrino Experiment: Exploring Fundamental Symmetries of the Universe
The preponderance of matter over antimatter in the early Universe, the
dynamics of the supernova bursts that produced the heavy elements necessary for
life and whether protons eventually decay --- these mysteries at the forefront
of particle physics and astrophysics are key to understanding the early
evolution of our Universe, its current state and its eventual fate. The
Long-Baseline Neutrino Experiment (LBNE) represents an extensively developed
plan for a world-class experiment dedicated to addressing these questions. LBNE
is conceived around three central components: (1) a new, high-intensity
neutrino source generated from a megawatt-class proton accelerator at Fermi
National Accelerator Laboratory, (2) a near neutrino detector just downstream
of the source, and (3) a massive liquid argon time-projection chamber deployed
as a far detector deep underground at the Sanford Underground Research
Facility. This facility, located at the site of the former Homestake Mine in
Lead, South Dakota, is approximately 1,300 km from the neutrino source at
Fermilab -- a distance (baseline) that delivers optimal sensitivity to neutrino
charge-parity symmetry violation and mass ordering effects. This ambitious yet
cost-effective design incorporates scalability and flexibility and can
accommodate a variety of upgrades and contributions. With its exceptional
combination of experimental configuration, technical capabilities, and
potential for transformative discoveries, LBNE promises to be a vital facility
for the field of particle physics worldwide, providing physicists from around
the globe with opportunities to collaborate in a twenty to thirty year program
of exciting science. In this document we provide a comprehensive overview of
LBNE's scientific objectives, its place in the landscape of neutrino physics
worldwide, the technologies it will incorporate and the capabilities it will
possess.Comment: Major update of previous version. This is the reference document for
LBNE science program and current status. Chapters 1, 3, and 9 provide a
comprehensive overview of LBNE's scientific objectives, its place in the
landscape of neutrino physics worldwide, the technologies it will incorporate
and the capabilities it will possess. 288 pages, 116 figure
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