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

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

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

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

Anderson localization in Bragg-guiding arrays with negative defects

We show that Anderson localization is possible in waveguide arrays with periodically-spaced defect waveguides having lower refractive index. Such localization is mediated by Bragg reflection, and it takes place even if diagonal or off-diagonal disorder affects only defect waveguides. For off-diagonal disorder the localization degree of the intensity distributions monotonically grows with increasing disorder. In contrast, under appropriate conditions, increasing diagonal disorder may result in weaker localization.Comment: 4 pages, 5 figures, to appear in Optics Letter

Cognitive and emotional empathy in individuals at clinical high risk of psychosis

Background Impairments of social cognition are considered core features of schizophrenia and are established predictors of social functioning. However, affective aspects of social cognition including empathy have far less been studied than its cognitive dimensions. The role of empathy in the development of schizophrenia remains largely elusive. Methods Emotional and cognitive empathy were investigated in large sample of 120 individuals at Clinical High Risk of Psychosis (CHR-P) and compared with 50 patients with schizophrenia and 50 healthy controls. A behavioral empathy assessment, the Multifaceted Empathy Test, was implemented, and associations of empathy with cognition, social functioning, and symptoms were determined. Results Our findings demonstrated significant reductions of emotional empathy in individuals at CHR-P, while cognitive empathy appeared intact. Only individuals with schizophrenia showed significantly reduced scores of cognitive empathy compared to healthy controls and individuals at CHR-P. Individuals at CHR-P were characterized by significantly lower scores of emotional empathy and unspecific arousal for both positive and negative affective valences compared to matched healthy controls and patients with schizophrenia. Results also indicated a correlation of lower scores of emotional empathy and arousal with higher scores of prodromal symptoms. Conclusion Findings suggest that the tendency to 'feel with' an interaction partner is reduced in individuals at CHR-P. Altered emotional reactivity may represent an additional, early vulnerability marker, even if cognitive mentalizing is grossly unimpaired in the prodromal stage. Different mechanisms might contribute to reductions of cognitive and emotional empathy in different stages of non-affective psychotic disorders and should be further explored

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