Contents

15 April 2014
Vol 7, Issue 321
  • Contents

    • Research Articles

    • Podcast

    • Editors' Choice

      • T Cells Hurt the Brain

        Blocking interleukin-21 signaling may alleviate the tissue damage caused by T cells that infiltrate the brain early after ischemic stroke.

      • In the PINK1

        Mitochondria lacking a Parkinson’s disease–associated kinase harbor a functionally important phosphorylation defect.

      • Pattern Recognition Receptor Antagonism

        A pathogenic fungus activates two C-type lectin receptors to skew the T cell response to one favorable to infection.

      • More Myeloid Cells, STAT!

        Hematopoietic stem and progenitor cells and mesenchymal stromal cells in the bone marrow use cytokines to respond to an acute need for more myeloid cells.

      • Ironing Out the Details with Autophagy

        NCOA4 acts as a cargo adaptor protein to enable selective autophagy of ferritin, thereby regulating iron bioavailability.

      • Nuclei Sense the Force

        Isolated nuclei can directly sense mechanical force and stimulate the phosphorylation of a nuclear membrane protein.

      • Shutting Down Repair to Protect

        Blocking two crucial repair factors prevents DNA repair during mitosis, which saves the cell from catastrophic chromosome fusions.

      • Tripeptide Maternal Support

        Within plant seeds, signaling functions from the endosperm regulate development of the embryonic plant suspensor.

      • Yeasty HIPHOP

        Guilt by association helps identify the chemogenomic signatures of compounds targeting yeast genes.

      • Contact Regulation of Heterogeneity

        Interactions with extracellular matrix alter dynamic transcriptional circuits in a cultured breast epithelial cell line, resulting in the appearance of cellular heterogeneity resembling that seen in breast tumors.

About The Cover

Cover image expansion

Online Cover This week features a Research Article that describes a double-lock autoinhibitory mechanism that prevents inappropriate activation of the guanine nucleotide exchange factor Vav1. The image shows the three-dimensional structure of part of Vav1 as determined by electron microscopy analysis, with the the region that forms one part of the double-lock shown in red. [Image: Eva Torreira and Oscar Llorca, CSIC, Madrid, Spain; and Xosé R. Bustelo, University of Salamanca, Salamanca, Spain]