News from the Broad

The Broad Institute is committed to open sharing not only of its scientific data and tools, but also information and news about our progress towards achieving our mission. Below are just a few highlights from the Broad scientific community.
  • Study identifies mechanism by which hydroxamate-based HDAC inhibitors protect neurons from oxidative stress

    April 30th, 2015

    The development of histone deacetylase inhibitors to treat a variety of diseases has been somewhat hampered by HDAC-related toxicity concerns. A team from the Stanley Center for Psychiatric Research at Broad Institute, led by the Center’s director of medicinal chemistry Ed Holson and Broad postdoctoral associate David Olson, has discovered a new HDAC-independent mechanism by which some hydroxamate-based HDAC inhibitors protect neurons from oxidative stress, such as during stroke.

  • Fine mapping of MHC region leads to identification of new genetic risk factors for celiac disease

    April 29th, 2015

    In a study published online last week in Nature Genetics, a team led by Broad visiting scientist Paul de Bakker of University Medical Center Utrecht fine mapped the major histocompatibility complex (MHC) – a linked set of genetic loci known to influence the development of celiac disease. The team’s approach turned up five new associated genetic variants that together account for roughly 18% of the genetic risk for the disease. Combined with previously identified risk factors, these genetic loci can now explain up to 48% of celiac disease heritability.

  • Study investigates biological pathways involved in inflammatory response to stress

    April 22nd, 2015

    A recent paper by Broad associate member Gökhan Hotamisligil, first author Takahisa Nakamura of Harvard T.H. Chan School of Public Health and Cincinnati Children’s Hospital Medical Center, and colleagues identifies components of a pathway— including a complex between double-stranded RNA-dependent kinase (PKR) and TAR RNA-binding protein (TRBP)—that integrates metabolic cues, stress signals, translational regulation, and the metabolically driven inflammatory response in obesity-related pathogenesis. These findings uncover a potential link between RNA metabolism and endogenous dsRNA-mediated signaling in the initiation and maintenance of a metabolic inflammatory state and provide potential targets for the treatment of chronic stress-related diseases including obesity-induced metabolic diseases. Their paper can be found online in Cell Reports.

  • New method characterizes amplification bias in single-cell genomic DNA

    April 21st, 2015

    In Nature Communications, a team led by researchers from the Broad Institute, MIT, and Dana-Farber Cancer Center describes new statistical methods that account for artifacts introduced by whole-genome amplification of single-cell genomic DNA. Their approach establishes a system for characterizing amplification bias and provides a framework for quality assurance in single-cell DNA libraries. Broad associate member J. Christopher Love and institute member Matthew Meyerson were senior authors of the study; Broad researchers Cheng-Zhong Zhang and Viktor Adalsteinsson were first authors.

  • New computational strategy maps single-cell spatial patterning in complex tissue

    April 17th, 2015

    For cells, location is key to their fate and behavior, but studying expression patterns across complex tissues is difficult. A team led by Broad visiting scientist Rahul Satija (of Broad core member Aviv Regev's lab) and Jeff Farrell (a postdoc in associate member Alex Schier's lab) recently reported on Seurat, their new computational strategy to map single cells by integrating single-cell RNA-seq data with RNA patterns from tissues. Their team used the tool, named after the 19th century pointillist painter, to generate a transcriptome-wide map of spatial patterning in zebrafish embryos, demonstrating Seurat's utility for mapping cells within complex patterned tissues. Their paper appears online in Nature Biotechnology.