Bath-induced decay of Stark many-body localization

We investigate the relaxation dynamics of an interacting Stark-localized system coupled to a dephasing bath, and compare its behavior to the conventional disorder-induced many body localized system. Specifically, we study the dynamics of population imbalance between even and odd sites, and the growth of the von Neumann entropy. For a large potential gradient, the imbalance is found to decay on a time scale that grows quadratically with the Wannier-Stark tilt. For the non-interacting system, it shows an exponential decay, which becomes a stretched exponential decay in the presence of finite interactions. This is different from a system with disorder-induced localization, where the imbalance exhibits a stretched exponential decay also for vanishing interactions. As another clear qualitative difference, we do not find a logarithmically slow growth of the von-Neumann entropy as it is found for the disordered system. Our findings can immediately be tested experimentally with ultracold atoms in optical lattices

Prethermal memory loss in interacting quantum systems coupled to thermal baths

We study the relaxation dynamics of an extended Fermi-Hubbard chain with a strong Wannier-Stark potential tilt coupled to a bath. When the system is subjected to dephasing noise, starting from a pure initial state the system's total von Neumann entropy is found to grow monotonously. The scenario becomes rather different when the system is coupled to a thermal bath of finite temperature. Here, for sufficiently large field gradients and initial energies, the entropy peaks in time and almost reaches its largest possible value (corresponding to the maximally mixed state), long before the system relaxes to thermal equilibrium. This entropy peak signals a prethermal memory loss and, relative to the time where it occurs, the system is found to exhibit a simple scaling behavior in space and time. By comparing the system's dynamics to that of a simplified model, the underlying mechanism is found to be related to the localization property of the Wannier-Stark system, which favors dissipative coupling between eigenstates that are close in energy

Heat transport in an optical lattice via Markovian feedback control

Ultracold atoms offer a unique opportunity to study many-body physics in a clean and well-controlled environment. However, the isolated nature of quantum gases makes it difficult to study transport properties of the system, which are among the key observables in condensed matter physics. In this work, we employ Markovian feedback control to synthesize two effective thermal baths that couple to the boundaries of a one-dimensional Bose-Hubbard chain. This allows for the realization of a heat-current-carrying state. We investigate the steady-state heat current, including its scaling with system size and its response to disorder. In order to study large systems, we use semi-classical Monte-Carlo simulation and kinetic theory. The numerical results from both approaches show, as expected, that for non- and weakly interacting systems with and without disorder one finds the same scaling of the heat current with respect to the system size as it is found for systems coupled to thermal baths. Finally, we propose and test a scheme for measuring the energy flow. Thus, we provide a route for the quantum simulation of heat-current-carrying steady states of matter in atomic quantum gases

Describing many-body localized systems in thermal environments

In this work we formulate an efficient method for the description of many-body localized systems in weak contact with thermal environments at temperature $T$. For this purpose we exploit the representation of the system in terms of quasi-local integrals of motion ($l$-bits) to derive a quantum master equation using Born-Markov approximations. We show how this equation can be treated by using quantum-jump Monte-Carlo techniques as well as by deriving approximate kinetic equations of motion. As an example, we consider the one-dimensional Anderson model for spinless fermions including also nearest-neighbor interactions, which we diagonalize approximately by employing a recently proposed method valid in the limit of strong disorder and weak interactions. Coupling the system to a global thermal bath, we study the transport between two leads with different chemical potentials at both of its ends. We find that the temperature-dependent current is captured by an interaction-dependent version of Mott's law for variable range hopping, where transport is enhanced/lowered depending on whether the interactions are attractive or repulsive, respectively. We interpret these results in terms of spatio-energetic correlations between the $l$-bits

Indication of critical scaling in time during the relaxation of an open quantum system

Phase transitions correspond to the singular behavior of physical systems in response to continuous control parameters like temperature or external fields. Near continuous phase transitions, associated with the divergence of a correlation length, universal power-law scaling behavior with critical exponents independent of microscopic system details is found. Recently, dynamical quantum phase transitions and universal scaling have been predicted and also observed in the non-equilibrium dynamics of isolated quantum systems after a quench, with time playing the role of the control parameter. However, signatures of such critical phenomena in time in open systems, whose dynamics is driven by the dissipative contact to an environment, were so far elusive. Here, we present results indicating that critical scaling with respect to time can also occur during the relaxation dynamics of an open quantum system described by mixed states. We experimentally measure the relaxation dynamics of the large atomic spin of individual Caesium atoms induced by the dissipative coupling via spin-exchange processes to an ultracold Bose gas of Rubidium atoms. For initial states far from equilibrium, the entropy of the spin state is found to peak in time, transiently approaching its maximum possible value, before eventually relaxing to its lower equilibrium value. Moreover, a finite-size scaling analysis based on numerical simulations shows that it corresponds to a critical point with respect to time of the dissipative system in the limit of large system sizes. It is signalled by the divergence of a characteristic length at a critical time, characterized by critical exponents that are found to be independent of system details

Knockdown of SF-1 and RNF31 Affects Components of Steroidogenesis, TGFβ, and Wnt/β-catenin Signaling in Adrenocortical Carcinoma Cells

The orphan nuclear receptor Steroidogenic Factor-1 (SF-1, NR5A1) is a critical regulator of development and homeostasis of the adrenal cortex and gonads. We recently showed that a complex containing E3 ubiquitin ligase RNF31 and the known SF-1 corepressor DAX-1 (NR0B1) interacts with SF-1 on target promoters and represses transcription of steroidogenic acute regulatory protein (StAR) and aromatase (CYP19) genes. To further evaluate the role of SF-1 in the adrenal cortex and the involvement of RNF31 in SF-1-dependent pathways, we performed genome-wide gene-expression analysis of adrenocortical NCI-H295R cells where SF-1 or RNF31 had been knocked down using RNA interference. We find RNF31 to be deeply connected to cholesterol metabolism and steroid hormone synthesis, strengthening its role as an SF-1 coregulator. We also find intriguing evidence of negative crosstalk between SF-1 and both transforming growth factor (TGF) β and Wnt/β-catenin signaling. This crosstalk could be of importance for adrenogonadal development, maintenance of adrenocortical progenitor cells and the development of adrenocortical carcinoma. Finally, the SF-1 gene profile can be used to distinguish malignant from benign adrenocortical tumors, a finding that implicates SF-1 in the development of malignant adrenocortical carcinoma

The Arabidopsis RNA Polymerase II Carboxyl Terminal Domain (CTD) Phosphatase-Like1 (CPL1) is a biotic stress susceptibility gene

© 2018, The Author(s). Crop breeding for improved disease resistance may be achieved through the manipulation of host susceptibility genes. Previously we identified multiple Arabidopsis mutants known as enhanced stress response1 (esr1) that have defects in a KH-domain RNA-binding protein and conferred increased resistance to the root fungal pathogen Fusarium oxysporum. Here, screening the same mutagenized population we discovered two further enhanced stress response mutants that also conferred enhanced resistance to F. oxysporum. These mutants also have enhanced resistance to a leaf fungal pathogen (Alternaria brassicicola) and an aphid pest (Myzus persicae), but not to the bacterial leaf pathogen Pseudomonas syringae. The causal alleles in these mutants were found to have defects in the ESR1 interacting protein partner RNA Polymerase II Carboxyl Terminal Domain (CTD) Phosphatase-Like1 (CPL1) and subsequently given the allele symbols cpl1-7 and cpl1-8. These results define a new role for CPL1 as a pathogen and pest susceptibility gene. Global transcriptome analysis and oxidative stress assays showed these cpl1 mutants have increased tolerance to oxidative stress. In particular, components of biotic stress responsive pathways were enriched in cpl1 over wild-type up-regulated gene expression datasets including genes related to defence, heat shock proteins and oxidative stress/redox state processes

Molecular Genetic Features of Polyploidization and Aneuploidization Reveal Unique Patterns for Genome Duplication in Diploid Malus

Polyploidization results in genome duplication and is an important step in evolution and speciation. The Malus genome confirmed that this genus was derived through auto-polyploidization, yet the genetic and meiotic mechanisms for polyploidization, particularly for aneuploidization, are unclear in this genus or other woody perennials. In fact the contribution of aneuploidization remains poorly understood throughout Plantae. We add to this knowledge by characterization of eupolyploidization and aneuploidization in 27,542 F1 seedlings from seven diploid Malus populations using cytology and microsatellite markers. We provide the first evidence that aneuploidy exceeds eupolyploidy in the diploid crosses, suggesting aneuploidization is a leading cause of genome duplication. Gametes from diploid Malus had a unique combinational pattern; ova preserved euploidy exclusively, while spermatozoa presented both euploidy and aneuploidy. All non-reduced gametes were genetically heterozygous, indicating first-division restitution was the exclusive mode for Malus eupolyploidization and aneuploidization. Chromosome segregation pattern among aneuploids was non-uniform, however, certain chromosomes were associated for aneuploidization. This study is the first to provide molecular evidence for the contribution of heterozygous non-reduced gametes to fitness in polyploids and aneuploids. Aneuploidization can increase, while eupolyploidization may decrease genetic diversity in their newly established populations. Auto-triploidization is important for speciation in the extant Malus. The features of Malus polyploidization confer genetic stability and diversity, and present heterozygosity, heterosis and adaptability for evolutionary selection. A protocol using co-dominant markers was proposed for accelerating apple triploid breeding program. A path was postulated for evolution of numerically odd basic chromosomes. The model for Malus derivation was considerably revised. Impacts of aneuploidization on speciation and evolution, and potential applications of aneuploids and polyploids in breeding and genetics for other species were evaluated in depth. This study greatly improves our understanding of evolution, speciation, and adaptation of the Malus genus, and provides strategies to exploit polyploidization in other species

Liver and Muscle in Morbid Obesity: The Interplay of Fatty Liver and Insulin Resistance

INTRODUCTION: Nonalcoholic fatty liver disease (NAFLD) can be seen as a manifestation of overnutrition. The muscle is a central player in the adaptation to energy overload, and there is an association between fatty-muscle and -liver. We aimed to correlate muscle morphology, mitochondrial function and insulin signaling with NAFLD severity in morbid obese patients. METHODS: Liver and deltoid muscle biopsies were collected during bariatric surgery in NAFLD patients. NAFLD Activity Score and Younossi's classification for nonalcoholic steatohepatitis (NASH) were applied to liver histology. Muscle evaluation included morphology studies, respiratory chain complex I to IV enzyme assays, and analysis of the insulin signaling cascade. A healthy lean control group was included for muscle morphology and mitochondrial function analyses. RESULTS: Fifty one NAFLD patients were included of whom 43% had NASH. Intramyocellular lipids (IMCL) were associated with the presence of NASH (OR 12.5, p<0.001), progressive hepatic inflammation (p = 0.029) and fibrosis severity (p = 0.010). There was a trend to an association between IMCL and decreased Akt phosphorylation (p = 0.059), despite no association with insulin resistance. In turn, hepatic steatosis (p = 0.015) and inflammation (p = 0.013) were associated with decreased Akt phosphoryation. Citrate synthase activity was lower in obese patients (p = 0.047) whereas complex I (p = 0.040) and III (p = 0.036) activities were higher, compared with controls. Finally, in obese patients, complex I activity increased with progressive steatosis (p = 0.049) and with a trend with fibrosis severity (p = 0.056). CONCLUSIONS: In morbid obese patients, presence of IMCL associates with NASH and advanced fibrosis. Muscle mitochondrial dysfunction does not appear to be a major driving force contributing to muscle fat accumulation, insulin resistance or liver disease. Importantly, insulin resistance in muscle might occur at a late point in the insulin signaling cascade and be associated with IMCL and NAFLD severity