Summarising the points made in online political debates

Online communities host growing numbers of discussions amongst large groups of participants on all manner of topics. This user-generated content contains millions of statements of opinions and ideas. We propose an abstractive approach to summarize such argumentative discussions, making key content accessible through ‘point’ extraction, where a point is a verb and its syntactic arguments. Our approach uses both dependency parse information and verb case frames to identify and extract valid points, and generates an abstractive summary that discusses the key points being made in the debate. We performed a human evaluation of our approach using a corpus of online political debates and report significant improvements over a high-performing extractive summarizer

Working paper 18: Prescribed and wildland use fires in the southwest: Do frequency and timing matter?

Support for the use of prescribed fire and wildland fire use has increased in the Southwest in recent decades. However, the frequency and seasonality of these contemporary fires is typically different than historical fires, which burned during late spring and early summer in the driest and windiest time of the year. Contemporary changes in the landscape, including unprecedented fuel loads and human development in and around forests, now limit the ability to use fire during those times of the year. Most managed fire now occurs outside the windy fire season because it is safer and allows managers to provide greater protection to susceptible cultural or natural resources, such as historic structures or dry snags

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

An Alternative Approach to ChIP-Seq Normalization Enables Detection of Genome-Wide Changes in Histone H3 Lysine 27 Trimethylation upon EZH2 Inhibition

<div><p>Chromatin immunoprecipitation and DNA sequencing (ChIP-seq) has been instrumental in inferring the roles of histone post-translational modifications in the regulation of transcription, chromatin compaction and other cellular processes that require modulation of chromatin structure. However, analysis of ChIP-seq data is challenging when the manipulation of a chromatin-modifying enzyme significantly affects global levels of histone post-translational modifications. For example, small molecule inhibition of the methyltransferase EZH2 reduces global levels of histone H3 lysine 27 trimethylation (H3K27me3). However, standard ChIP-seq normalization and analysis methods fail to detect a decrease upon EZH2 inhibitor treatment. We overcome this challenge by employing an alternative normalization approach that is based on the addition of <i>Drosophila melanogaster</i> chromatin and a <i>D</i>. <i>melanogaster-</i>specific antibody into standard ChIP reactions. Specifically, the use of an antibody that exclusively recognizes the <i>D</i>. <i>melanogaster</i> histone variant H2Av enables precipitation of <i>D</i>. <i>melanogaster</i> chromatin as a minor fraction of the total ChIP DNA. The <i>D</i>. <i>melanogaster</i> ChIP-seq tags are used to normalize the human ChIP-seq data from DMSO and EZH2 inhibitor-treated samples. Employing this strategy, a substantial reduction in H3K27me3 signal is now observed in ChIP-seq data from EZH2 inhibitor treated samples.</p></div

Reduced H3K27me3 binding is detected by ChIP-qPCR.

<p><b>(A)</b> ChIP was performed using chromatin from KARPAS-422 cells treated with the EZH2 inhibitor CPI-360. qPCR using the positive control primer <i>MYT1</i> showed reduced H3K27me3 occupancy in the presence of the inhibitor. <b>(B)</b> ChIP was performed using chromatin from PC9 cells treated with the EZH2 inhibitor GSK126. qPCR using the positive control primer <i>MYT1</i> showed reduced H3K27me3 occupancy in cells treated with the inhibitor. (<b>C</b>) Libraries were generated from KARPAS-422 cells using 15 cycles of PCR amplification. Library DNA was diluted and qPCR was performed using positive control primers for <i>MYT1</i> and <i>CCND2</i>. (<b>D</b>) Libraries were generated from PC9 cells as described in (C) and library DNA was used for qPCR using positive control primers for <i>MYT1</i> and <i>CCND2</i>. All experiments are represented as the mean of two independent experiments with qPCRs performed in triplicate ±SD. The <i>ACTB</i> promoter served as a negative control for all experiments.</p

EZH2 inhibition reduces global H3K27me3 levels, however standard ChIP-seq methods do not reveal the reduction.

<p><b>(A)</b> Western blot showing reduced global H3K27me3 levels in KARPAS-422 cells treated with 1.5 μM CPI-360 for 4 and 8 days. Whole cell extracts were resolved by SDS page and immuno-blotted with anti-H3K27me3. Anti-H3 immuno-blots show equal levels of total H3. <b>(B)</b> Western blot showing reduced global H3K27me3 levels in PC9 cells treated with 1 μM of GSK126 for 5 days. Whole cell extracts were resolved by SDS page and immuno-blotted with anti-H3K27me3. Anti-H3 immuno-blots show equal levels of total H3. <b>(C, D)</b> Representation of H3K27me3 ChIP-seq data using IGV. No obvious differences are detected in CPI-360 (C) and GSK126 (D) treated KARPAS-422 and PC9 cells when compared to vehicle-treated controls. <b>(E, F)</b> Genome-wide data from H3K27me3 ChIP-seq experiments under different treatment conditions are represented as scatter plots.</p

Schematic representation of the ChIP-seq spike-in protocol.

<p>ChIP-seq spike-in reactions are set up by adding the test chromatin of interest (human or other), the target antibody of interest, a small portion of <i>D</i>. <i>melanogaster</i> chromatin and the <i>D</i>. <i>melanogaster-</i>H2Av-specific antibody. The <i>D</i>. <i>melanogaster</i> spike-in chromatin is added in equal amounts and the H2Av antibody functions to pull down a small portion of the <i>D</i>. <i>melanogaster</i> chromatin in each reaction. After sequencing, tags are mapped to the genome corresponding to the test chromatin as well as to the <i>D</i>. <i>melanogaster</i> genome. The total number of tags uniquely mapping to the <i>D</i>. <i>melanogaster</i> genome are counted for each sample and used to generate correction factors (DMSO tags/inhibitor tags). The test chromatin tag counts are then normalized using the correction factors.</p