UCL  IRIS
Institutional Research Information Service
UCL Logo
Please report any queries concerning the funding data grouped in the sections named "Externally Awarded" or "Internally Disbursed" (shown on the profile page) to your Research Finance Administrator. Your can find your Research Finance Administrator at https://www.ucl.ac.uk/finance/research/rs-contacts.php by entering your department
Please report any queries concerning the student data shown on the profile page to:

Email: portico-services@ucl.ac.uk

Help Desk: http://www.ucl.ac.uk/ras/portico/helpdesk
Publication Detail
Actin is an evolutionarily-conserved damage-associated molecular pattern that signals tissue injury in Drosophila melanogaster.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Srinivasan N, Gordon O, Ahrens S, Franz A, Deddouche S, Chakravarty P, Phillips D, Yunus AA, Rosen MK, Valente RS, Teixeira L, Thompson B, Dionne MS, Wood W, Reis e Sousa C
  • Publication date:
    22/11/2016
  • Journal:
    Elife
  • Volume:
    5
  • Status:
    Published online
  • Country:
    England
  • Language:
    eng
  • Keywords:
    D. melanogaster, DAMP, JAK/STAT pathway, damage-associated molecular pattern, immunology, innate immunity, sterile inflammation, tissue injury, Actins, Alarmins, Animals, Drosophila melanogaster, Signal Transduction, Stress, Physiological
Abstract
Damage-associated molecular patterns (DAMPs) are molecules released by dead cells that trigger sterile inflammation and, in vertebrates, adaptive immunity. Actin is a DAMP detected in mammals by the receptor, DNGR-1, expressed by dendritic cells (DCs). DNGR-1 is phosphorylated by Src-family kinases and recruits the tyrosine kinase Syk to promote DC cross-presentation of dead cell-associated antigens. Here we report that actin is also a DAMP in invertebrates that lack DCs and adaptive immunity. Administration of actin to Drosophila melanogaster triggers a response characterised by selective induction of STAT target genes in the fat body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless. Notably, this response requires signalling via Shark, the Drosophila orthologue of Syk, and Src42A, a Drosophila Src-family kinase, and is dependent on Nox activity. Thus, extracellular actin detection via a Src-family kinase-dependent cascade is an ancient means of detecting cell injury that precedes the evolution of adaptive immunity.
Publication data is maintained in RPS. Visit https://rps.ucl.ac.uk
 More search options
UCL Researchers
Author
Cell & Developmental Biology
University College London - Gower Street - London - WC1E 6BT Tel:+44 (0)20 7679 2000

© UCL 1999–2011

Search by