Exactly solvable approximating models for Rabi Hamiltonian dynamics

The interaction between an atom and a one mode external driving field is an ubiquitous problem in many branches of physics and is often modeled using the Rabi Hamiltonian. In this paper we present a series of analytically solvable Hamiltonians that approximate the Rabi Hamiltonian and compare our results to the Jaynes-Cummings model which neglects the so-called counter-rotating term in the Rabi Hamiltonian. Through a unitary transformation that diagonlizes the Jaynes-Cummings model, we transform the counter-rotating term into separate terms representing several different physical processes. By keeping only certain terms, we can achieve an excellent approximation to the exact dynamics within specified parameter ranges

Selective impairment of methylation maintenance is the major cause of DNA methylation reprogramming in the early embryo

DNA methylomes are extensively reprogrammed during mouse pre-implantation and early germ cell development. The main feature of this reprogramming is a genome-wide decrease in 5-methylcytosine (5mC). Standard high-resolution single-stranded bisulfite sequencing techniques do not allow discrimination of the underlying passive (replication-dependent) or active enzymatic mechanisms of 5mC loss. We approached this problem by generating high-resolution deep hairpin bisulfite sequencing (DHBS) maps, allowing us to follow the patterns of symmetric DNA methylation at CpGs dyads on both DNA strands over single replications.We compared DHBS maps of repetitive elements in the developing zygote, the early embryo, and primordial germ cells (PGCs) at defined stages of development. In the zygote, we observed distinct effects in paternal and maternal chromosomes. A significant loss of paternal DNA methylation was linked to replication and to an increase in continuous and dispersed hemimethylated CpG dyad patterns. Overall methylation levels at maternal copies remained largely unchanged, but showed an increased level of dispersed hemi-methylated CpG dyads. After the first cell cycle, the combined DHBS patterns of paternal and maternal chromosomes remained unchanged over the next three cell divisions. By contrast, in PGCs the DNA demethylation process was continuous, as seen by a consistent decrease in fully methylated CpG dyads over consecutive cell divisions.The main driver of DNA demethylation in germ cells and in the zygote is partial impairment of maintenance of symmetric DNA methylation at CpG dyads. In the embryo, this passive demethylation is restricted to the first cell division, whereas it continues over several cell divisions in germ cells. The dispersed patterns of CpG dyads in the early-cleavage embryo suggest a continuous partial (and to a low extent active) loss of methylation apparently compensated for by selective de novo methylation. We conclude that a combination of passive and active demethylation events counteracted by de novo methylation are involved in the distinct reprogramming dynamics of DNA methylomes in the zygote, the early embryo, and PGCs

Time evolution of the Rabi Hamiltonian from the unexcited vacuum

The Rabi Hamiltonian describes a single mode of electromagnetic radiation interacting with a two-level atom. Using the coupled cluster method, we investigate the time evolution of this system from an initially empty field mode and an unexcited atom. We give results for the atomic inversion and field occupation, and find that the virtual processes cause the field to be squeezed. No anti-bunching occurs.Comment: 25 pages, 8 figures, RevTe

A global disorder of imprinting in the human female germ line

Imprinted genes are expressed differently depending on whether they are carried by a chromosome of maternal or paternal origin. Correct imprinting is established by germline-specific modifications; failure of this process underlies several inherited human syndromes. All these imprinting control defects are cis-acting, disrupting establishment or maintenance of allele-specific epigenetic modifications across one contiguous segment of the genome. In contrast, we report here an inherited global imprinting defect. This recessive maternal-effect mutation disrupts the specification of imprints at multiple, non-contiguous loci, with the result that genes normally carrying a maternal methylation imprint assume a paternal epigenetic pattern on the maternal allele. The resulting conception is phenotypically indistinguishable from an androgenetic complete hydatidiform mole, in which abnormal extra-embryonic tissue proliferates while development of the embryo is absent or nearly so. This disorder offers a genetic route to the identification of trans-acting oocyte factors that mediate maternal imprint establishment

Geometric and dynamic perspectives on phase-coherent and noncoherent chaos

Statistically distinguishing between phase-coherent and noncoherent chaotic dynamics from time series is a contemporary problem in nonlinear sciences. In this work, we propose different measures based on recurrence properties of recorded trajectories, which characterize the underlying systems from both geometric and dynamic viewpoints. The potentials of the individual measures for discriminating phase-coherent and noncoherent chaotic oscillations are discussed. A detailed numerical analysis is performed for the chaotic R\"ossler system, which displays both types of chaos as one control parameter is varied, and the Mackey-Glass system as an example of a time-delay system with noncoherent chaos. Our results demonstrate that especially geometric measures from recurrence network analysis are well suited for tracing transitions between spiral- and screw-type chaos, a common route from phase-coherent to noncoherent chaos also found in other nonlinear oscillators. A detailed explanation of the observed behavior in terms of attractor geometry is given.Comment: 12 pages, 13 figure

Functional integral treatment of some quantum nondemolition systems

In the scheme of a quantum nondemolition (QND) measurement, an observable is measured without perturbing its evolution. In the context of studies of decoherence in quantum computing, we examine the `open' quantum system of a two-level atom, or equivalently, a spin-1/2 system, in interaction with quantum reservoirs of either oscillators or spins, under the QND condition of the Hamiltonian of the system commuting with the system-reservoir interaction. For completeness, we also examine the well-known non-QND spin-Bose problem. For all these many-body systems, we use the methods of functional integration to work out the propagators. The propagators for the QND Hamiltonians are shown to be analogous to the squeezing and rotation operators, respectively, for the two kinds of baths considered. Squeezing and rotation being both phase space area-preserving canonical transformations, this brings out an interesting connection between the energy-preserving QND Hamiltonians and the homogeneous linear canonical transformations.Comment: 16 pages, no figure

TET3 prevents terminal differentiation of adult NSCs by a non-catalytic action at Snrpn.

Ten-eleven-translocation (TET) proteins catalyze DNA hydroxylation, playing an important role in demethylation of DNA in mammals. Remarkably, although hydroxymethylation levels are high in the mouse brain, the potential role of TET proteins in adult neurogenesis is unknown. We show here that a non-catalytic action of TET3 is essentially required for the maintenance of the neural stem cell (NSC) pool in the adult subventricular zone (SVZ) niche by preventing premature differentiation of NSCs into non-neurogenic astrocytes. This occurs through direct binding of TET3 to the paternal transcribed allele of the imprinted gene Small nuclear ribonucleoprotein-associated polypeptide N (Snrpn), contributing to transcriptional repression of the gene. The study also identifies BMP2 as an effector of the astrocytic terminal differentiation mediated by SNRPN. Our work describes a novel mechanism of control of an imprinted gene in the regulation of adult neurogenesis through an unconventional role of TET3

Germline Mutation in NLRP2 (NALP2) in a Familial Imprinting Disorder (Beckwith-Wiedemann Syndrome)

Beckwith-Wiedemann syndrome (BWS) is a fetal overgrowth and human imprinting disorder resulting from the deregulation of a number of genes, including IGF2 and CDKN1C, in the imprinted gene cluster on chromosome 11p15.5. Most cases are sporadic and result from epimutations at either of the two 11p15.5 imprinting centres (IC1 and IC2). However, rare familial cases may be associated with germline 11p15.5 deletions causing abnormal imprinting in cis. We report a family with BWS and an IC2 epimutation in which affected siblings had inherited different parental 11p15.5 alleles excluding an in cis mechanism. Using a positional-candidate gene approach, we found that the mother was homozygous for a frameshift mutation in exon 6 of NLRP2. While germline mutations in NLRP7 have previously been associated with familial hydatidiform mole, this is the first description of NLRP2 mutation in human disease and the first report of a trans mechanism for disordered imprinting in BWS. These observations are consistent with the hypothesis that NLRP2 has a previously unrecognised role in establishing or maintaining genomic imprinting in humans

Photoinduced IR absorption in (La(1-x)Sr(x)Mn)(1-\delta)O3: changes of the anti-Jahn-Teller polaron binding energy with doping

Photoinduced IR absorption was measured in (La(1-x)Sr(x)Mn)(1-\delta)O3. A midinfrared peak centered at ~ 5000 cm$^{-1}$ was observed in the x=0 antiferromagnetic sample. The peak diminishes and softens as hole doping is increased. The origin of the photoinduced absorption peak is atributted to the photon assisted hopping of anti-Jahn-Teller polarons formed by photoexcited charge carriers, whose binding energy decreases with increasing hole doping. The shape of the peak indicates that the polarons are small.Comment: 5 pages, 3 figures, submitted to PR

Dnmt2-dependent methylomes lack defined DNA methylation patterns

Several organisms have retained methyltransferase 2 (Dnmt2) as their only candidate DNA methyltransferase gene. However, information about Dnmt2-dependent methylation patterns has been limited to a few isolated loci and the results have been discussed controversially. In addition, recent studies have shown that Dnmt2 functions as a tRNA methyltransferase, which raised the possibility that Dnmt2-only genomes might be unmethylated. We have now used whole-genome bisulfite sequencing to analyze the methylomes of Dnmt2-only organisms at single-base resolution. Our results show that the genomes of Schistosoma mansoni and Drosophila melanogaster lack detectable DNA methylation patterns. Residual unconverted cytosine residues shared many attributes with bisulfite deamination artifacts and were observed at comparable levels in Dnmt2-deficient flies. Furthermore, genetically modified Dnmt2-only mouse embryonic stem cells lost the DNA methylation patterns found in wild-type cells. Our results thus uncover fundamental differences among animal methylomes and suggest that DNA methylation is dispensable for a considerable number of eukaryotic organisms