Modulations of DNA contacts by linker histones and post-translational modifications determine the mobility and modifiability of nucleosomal H3 tails.

Post-translational histone modifications and linker histone incorporation regulate chromatin structure and genome activity. How these systems interface on a molecular level is unclear. Using biochemistry and NMR spectroscopy, we deduced mechanistic insights into the modification behavior of N-terminal histone H3 tails in different nucleosomal contexts. We find that linker histones generally inhibit modifications of different H3 sites and reduce H3 tail dynamics in nucleosomes. These effects are caused by modulations of electrostatic interactions of H3 tails with linker DNA and largely depend on the C-terminal domains of linker histones. In agreement, linker histone occupancy and H3 tail modifications segregate on a genome-wide level. Charge-modulating modifications such as phosphorylation and acetylation weaken transient H3 tail-linker DNA interactions, increase H3 tail dynamics, and, concomitantly, enhance general modifiability. We propose that alterations of H3 tail-linker DNA interactions by linker histones and charge-modulating modifications execute basal control mechanisms of chromatin function

Mobility transition from ballistic to diffusive transport in non-Hermitian lattices

Within all physical disciplines, it is accepted that wave transport is predetermined by the existence of disorder. In this vein, it is known that ballistic transport is possible only when a structure is ordered, and that disorder is crucial for diffusion or (Anderson-)localization to occur. As this commonly accepted picture is based on the very foundations of quantum mechanics where Hermiticity of the Hamiltonian is naturally assumed, the question arises whether these concepts of transport hold true within the more general context of non-Hermitian systems. Here we demonstrate theoretically and experimentally that in ordered time-independent PT-symmetric systems, which are symmetric under space-time reflection, wave transport can undergo a sudden change from ballistic to diffusive after a specific point in time. This transition as well as the diffusive transport in general is impossible in Hermitian systems in the absence of disorder. In contrast, we find that this transition depends only on the degree of dissipation

Mobility transition from ballistic to diffusive transport in non-Hermitian lattices

Within all physical disciplines, it is accepted that wave transport is predetermined by the existence of disorder. In this vein, it is known that ballistic transport is possible only when a structure is ordered, and that disorder is crucial for diffusion or (Anderson-)localization to occur. As this commonly accepted picture is based on the very foundations of quantum mechanics where Hermiticity of the Hamiltonian is naturally assumed, the question arises whether these concepts of transport hold true within the more general context of non-Hermitian systems. Here we demonstrate theoretically and experimentally that in ordered time-independent PT-symmetric systems, which are symmetric under space-time reflection, wave transport can undergo a sudden change from ballistic to diffusive after a specific point in time. This transition as well as the diffusive transport in general is impossible in Hermitian systems in the absence of disorder. In contrast, we find that this transition depends only on the degree of dissipation

Observation of Bloch oscillations with a threshold

We demonstrate experimentally Bloch oscillations, which occur above a certain threshold value of the effective potential gradient in lattices with specially modulated coupling between the neighboring sites. We formulate the general conditions for this phenomenon, arising due to the competition between the tilting and broadening of the transmission band, and explain why no threshold was present in any previous observations. Our experiments are performed in inhomogeneous photonic lattices, which represent the process of quantum two-mode squeezing in Fock space, underpinning a fundamental quantum-classical correspondence

Anderson localization in a periodic photonic lattice with a disordered boundary

We investigate experimentally the light evolution inside a two-dimensional finite periodic array of weakly- coupled optical waveguides with a disordered boundary. For a completely localized initial condition away from the surface, we find that the disordered boundary induces an asymptotic localization in the bulk, centered around the initial position of the input beam.Comment: 3 pages, 4 figure

Experimental realization of a topological Anderson insulator

We experimentally demonstrate that disorder can induce a topologically non-trivial phase. We implement this “Topological Anderson Insulator” in arrays of evanescently coupled waveguides and demonstrate its unique features

Chromosome alterations in human hepatocellular carcinomas correlate with aetiology and histological grade – results of an explorative CGH meta-analysis

All available comparative genomic hybridisation (CGH) analyses (n=31, until 12/2003) of human hepatocellular carcinomas (HCCs; n=785) and premalignant dysplastic nodules (DNs; n=30) were compiled and correlated with clinical and histological parameters. The most prominent amplifications of genomic material were present in 1q (57.1%), 8q (46.6%), 6p (22.3%), and 17q (22.2%), while losses were most prevalent in 8p (38%), 16q (35.9%), 4q (34.3%), 17p (32.1%), and 13q (26.2%). Deletions of 4q, 16q, 13q, and 8p positively correlated with hepatitis B virus aetiology, while losses of 8p were more frequently found in hepatitis C virus-negative cases. In poorly differentiated HCCs, 13q and 4q were significantly under-represented. Moreover, gains of 1q were positively correlated with the occurrence of all other high-frequency alterations in HCCs. In DNs, amplifications were most frequently present in 1q and 8q, while deletions occurred in 8p, 17p, 5p, 13q, 14q, and 16q. In conclusion, aetiology and dedifferentiation correlate with specific genomic alterations in human HCCs. Gains of 1q appear to be rather early events that may predispose to further chromosomal abnormalities. Thus, explorative CGH meta-analysis generates novel and testable hypotheses regarding the cause and functional significance of genomic alterations in human HCCs

The pancreatic beta cell surface proteome

The pancreatic beta cell is responsible for maintaining normoglycaemia by secreting an appropriate amount of insulin according to blood glucose levels. The accurate sensing of the beta cell extracellular environment is therefore crucial to this endocrine function and is transmitted via its cell surface proteome. Various surface proteins that mediate or affect beta cell endocrine function have been identified, including growth factor and cytokine receptors, transporters, ion channels and proteases, attributing important roles to surface proteins in the adaptive behaviour of beta cells in response to acute and chronic environmental changes. However, the largely unknown composition of the beta cell surface proteome is likely to harbour yet more information about these mechanisms and provide novel points of therapeutic intervention and diagnostic tools. This article will provide an overview of the functional complexity of the beta cell surface proteome and selected surface proteins, outline the mechanisms by which their activity may be modulated, discuss the methods and challenges of comprehensively mapping and studying the beta cell surface proteome, and address the potential of this interesting subproteome for diagnostic and therapeutic applications in human disease