Search for: All records

Abstract Many-body effects play an important role in enhancing and modifying optical absorption and other excited-state properties of solids in the perturbative regime, but their role in high harmonic generation (HHG) and other nonlinear response beyond the perturbative regime is not well-understood. We develop here an ab initio many-body method to study nonperturbative HHG based on the real-time propagation of the non-equilibrium Green’s function with the GW self energy. We calculate the HHG of monolayer MoS₂and obtain good agreement with experiment, including the reproduction of characteristic patterns of monotonic and nonmonotonic harmonic yield in the parallel and perpendicular responses, respectively. Here, we show that many-body effects are especially important to accurately reproduce the spectral features in the perpendicular response, which reflect a complex interplay of electron-hole interactions (or exciton effects) in tandem with the many-body renormalization and Berry curvature of the independent quasiparticle bandstructure. 

Abstract DNA methylation at cytosine bases (5-methylcytosine, 5mC) is a heritable epigenetic mark regulating gene expression. While enzymes that metabolize 5mC are well-characterized, endogenous signaling molecules that regulate DNA methylation machinery have not been described. We report that physiological nitric oxide (NO) concentrations reversibly inhibit the DNA demethylases TET and ALKBH2 by binding to the mononuclear non-heme iron atom forming a dinitrosyliron complex (DNIC) and preventing cosubstrates from binding. In cancer cells treated with exogenous NO, or endogenously synthesizing NO, 5mC and 5-hydroxymethylcytosine (5hmC) increase, with no changes in DNA methyltransferase activity. 5mC is also significantly increased in NO-producing patient-derived xenograft tumors from mice. Genome-wide methylome analysis of cells chronically treated with NO (10 days) shows enrichment of 5mC and 5hmC at gene-regulatory loci, correlating with altered expression of NO-regulated tumor-associated genes. Regulation of DNA methylation is distinctly different from canonical NO signaling and represents a unique epigenetic role for NO.