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Datasets used in "Analyzing histone ChIP-seq data with a bin-based probability of being signal"

Datasets for reproducing figures from the manuscript "Analyzing histone ChIP-seq data with a bin-based probability of being signal"

In the version of this article initially published, two members of the ENCODE Project Consortium were missing from the author list. Rizi Ai (Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA, USA) and Shantao Li (Program in Computational Biology and Bioinformatics, Yale University, New Haven, CT, USA) are now included in the author list. These errors have been corrected in the online version of the article.

The human and mouse genomes contain instructions that specify RNAs and proteins and govern the timing, magnitude, and cellular context of their production. To better delineate these elements, phase III of the Encyclopedia of DNA Elements (ENCODE) Project has expanded analysis of the cell and tissue repertoires of RNA transcription, chromatin structure and modification, DNA methylation, chromatin looping, and occupancy by transcription factors and RNA-binding proteins. Here we summarize these efforts, which have produced 5,992 new experimental datasets, including systematic determinations across mouse fetal development. All data are available through the ENCODE data portal (https://www.encodeproject.org), including phase II ENCODE1 and Roadmap Epigenomics2 data. We have developed a registry of 926,535 human and 339,815 mouse candidate cis-regulatory elements, covering 7.9 and 3.4% of their respective genomes, by integrating selected datatypes associated with gene regulation, and constructed a web-based server (SCREEN; http://screen.encodeproject.org) to provide flexible, user-defined access to this resource. Collectively, the ENCODE data and registry provide an expansive resource for the scientific community to build a better understanding of the organization and function of the human and mouse genomes.

We construct the chiral effective Lagrangian for two lattice theories: one with Wilson fermions and the other with Wilson sea fermions and Ginsparg-Wilson valence fermions. For each of these theories we construct the Symanzik action through order $a^2$. The chiral Lagrangian is then derived, including terms of order $a^2$, which have not been calculated before. We find that there are only few new terms at this order. Corrections to existing coefficients in the continuum chiral Lagrangian are proportional to $a^2$, and appear in the Lagrangian at order $a^2 p^2$ or higher. Similarly, O(4) symmetry breaking terms enter the Symanzik action at order $a^2$, but contribute to the chiral Lagrangian at order $a^2 p^4$ or higher. We calculate the light meson masses in chiral perturbation theory for both lattice theories. At next-to-leading order, we find that there are no order $a^2$ corrections to the valence-valence meson mass in the mixed theory due to the enhanced chiral symmetry of the valence sector., Comment: 25 pages, LaTeX2e; references added

This paper completes the argument that lattice simulations of partially quenched QCD can provide quantitative information about QCD itself, with the aid of partially quenched chiral perturbation theory. A barrier to doing this has been the inclusion of $��_0$, the partially quenched generalization of the $��'$, in previous calculations in the partially quenched effective theory. This invalidates the low energy perturbative expansion, gives rise to many new unknown parameters, and makes it impossible to reliably calculate the relation between the partially quenched theory and low energy QCD. We show that it is straightforward and natural to formulate partially quenched chiral perturbation theory without $��_0$, and that the resulting theory contains the effective theory for QCD without the $��'$. We also show that previous results, obtained including $��_0$, can be reinterpreted as applying to the theory without $��_0$. We contrast the situation with that in the quenched effective theory, where we explain why it is necessary to include $��_0$. We also compare the derivation of chiral perturbation theory in partially quenched QCD with the standard derivation in unquenched QCD. We find that the former cannot be justified as rigorously as the latter, because of the absence of a physical Hilbert space. Finally, we present an encouraging result: unphysical double poles in certain correlation functions in partially quenched chiral perturbation theory can be shown to be a property of the underlying theory, given only the symmetries and some plausible assumptions., 45 pages, no figures

The effective field theory (EFT) for a toy model of nucleons interacting via a short range and a long range Yukawa potential is presented. The scattering amplitude in the 1S0 channel is calculated up to NNLO using KSW power counting scheme. A particular expansion of the amplitude about the pole at low (imaginary) momentum is used to derive matching conditions for the EFT couplings. In addition, after imposing constraints from a Renormalization Group analysis, there are no new free parameters in the amplitude at NNLO. Comparing the NNLO phase shifts to the full model we show that the EFT expansion is converging., Comment: 24 pages, 11 EPS figures, revtex; typos in formulae corrected; More typos corrected, expressions in appendix added, minor changes in style, graph Fig3(b) replaced

We introduce an approach to identify disease-relevant tissues and cell types by analyzing gene expression data together with genome-wide association study (GWAS) summary statistics. Our approach uses stratified linkage disequilibrium (LD) score regression to test whether disease heritability is enriched in regions surrounding genes with the highest specific expression in a given tissue. We applied our approach to gene expression data from several sources together with GWAS summary statistics for 48 diseases and traits (average N = 169,331) and found significant tissue-specific enrichments (false discovery rate (FDR) < 5%) for 34 traits. In our analysis of multiple tissues, we detected a broad range of enrichments that recapitulated known biology. In our brain-specific analysis, significant enrichments included an enrichment of inhibitory over excitatory neurons for bipolar disorder, and excitatory over inhibitory neurons for schizophrenia and body mass index. Our results demonstrate that our polygenic approach is a powerful way to leverage gene expression data for interpreting GWAS signals.