Background: CHD2 is a conserved ATPase and deletions of CHD2 have been linked to developmental and neurological disorders. Results:The regions flanking the ATPase domain of CHD2 confer substrate specificity and couple ATP hydrolysis to remodeling. Conclusion: CHD2 possesses nucleosome assembly activity regulated by its accessory domains. Significance: Understanding the mechanisms of chromatin remodeling is crucial for delineating how remodeling defects contribute to human diseases.

h i g h l i g h t s Photocatalytic, superhydrophobic and self-cleaning capabilities were promoted on asphalt mixtures. AC 6 and AC 14 mixtures were coated with TiO 2 and/or ZnO aqueous solutions by spraying. Physicochemical and morphological properties of bitumen samples were evaluated by FTIR and AFM. New pavement surface capabilities assessed with Water Angle Contact and Photocatalytic Efficiency tests. No deterioration was guaranteed for AC 14 TiO 2 , AC 14 TiO 2 ZnO, AC 6 TiO 2 and AC 6 TiO 2 ZnO solutions.

This work reports a computational study, focused on graphene (G) and graphene oxide (GO) interfaces with titanium dioxide (TiO 2), and an experimental assay on the photocatalytic activity of TiO 2 /G and TiO 2 /GO nanocomposites in the degradation of two different pollutants: methylene blue and ciprofloxacin. Both carbon nanostructures were compared due to their different chemical structure: GO is a G derivative with oxygen functional groups which should promote a closer chemical interaction with TiO 2 nanoparticles. Computational models of the fundamental properties of the composites indicated potentially improved photocatalytic activity compared to TiO 2 , namely lower band gaps and charge carrier segregation at the interfaces. These fundamental properties match qualitatively experimental results on methylene blue, which was more effectively degraded by TiO 2 /G and TiO 2 /GO nanocomposites than by pure TiO 2 under UV light. In contrast, the same nanocomposites were found to be less efficient to degrade ciprofloxacin than pure TiO 2 under visible and UV light. Therefore, this work showcases the relevance of an efficient matching between the catalyst and the molecular properties and structure of the pollutant.

CHD1 is a conserved chromatin remodeling enzyme required for development and linked to prostate cancer in adults, yet its role in human cells is poorly understood. Here, we show that targeted disruption of the CHD1 gene in human cells leads to a defect in early double-strand break (DSB) repair via homologous recombination (HR), resulting in hypersensitivity to ionizing radiation as well as PARP and PTEN inhibition. CHD1 knockout cells show reduced H2AX phosphorylation (γH2AX) and foci formation as well as impairments in CtIP recruitment to the damaged sites. Chromatin immunoprecipitation following a single DSB shows that the reduced levels of γH2AX accumulation at DSBs in CHD1-KO cells are due to both a global reduction in H2AX incorporation and poor retention of H2AX at the DSBs. We also identified a unique N-terminal region of CHD1 that inhibits the DNA binding, ATPase, and chromatin assembly and remodeling activities of CHD1. CHD1 lacking the N terminus was more active in rescuing the defects in γH2AX formation and CtIP recruitment in CHD1-KO cells than full-length CHD1, suggesting the N terminus is a negative regulator in cells. Our data point to a role for CHD1 in the DSB repair process and identify a novel regulatory region of the protein.