IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v6y2015i1d10.1038_ncomms8474.html
   My bibliography  Save this article

KDEL receptor 1 regulates T-cell homeostasis via PP1 that is a key phosphatase for ISR

Author

Listed:
  • Daisuke Kamimura

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Kokichi Katsunuma

    (Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Yasunobu Arima

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Toru Atsumi

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Jing-jing Jiang

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Hidenori Bando

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Jie Meng

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Lavannya Sabharwal

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Andrea Stofkova

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University)

  • Naoki Nishikawa

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University)

  • Hironao Suzuki

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Hideki Ogura

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Naoko Ueda

    (Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Mineko Tsuruoka

    (Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Masaya Harada

    (Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

  • Junya Kobayashi

    (Radiation Biology Center, Kyoto University)

  • Takanori Hasegawa

    (Laboratory for Developmental Genetics, RIKEN Research Center for Allergy and Immunology)

  • Hisahiro Yoshida

    (Laboratory for Immunogenetics, RIKEN Research Center for Allergy and Immunology)

  • Haruhiko Koseki

    (Laboratory for Developmental Genetics, RIKEN Research Center for Allergy and Immunology)

  • Ikuo Miura

    (Technology and Development Team for Mouse Phenotype Analysis, RIKEN Bioresource Center)

  • Shigeharu Wakana

    (Technology and Development Team for Mouse Phenotype Analysis, RIKEN Bioresource Center)

  • Keigo Nishida

    (Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology)

  • Hidemitsu Kitamura

    (Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology)

  • Toshiyuki Fukada

    (Laboratory for Cytokine Signaling, RIKEN Research Center for Allergy and Immunology)

  • Toshio Hirano

    (Osaka University)

  • Masaaki Murakami

    (Institute for Genetic Medicine and Graduate School of Medicine, Hokkaido University
    Laboratory of Developmental Immunology, Graduate School of Frontier Biosciences, Graduate School of Medicine, and WPI Immunology Frontier Research Center, Osaka University)

Abstract

KDEL receptors are responsible for retrotransporting endoplasmic reticulum (ER) chaperones from the Golgi complex to the ER. Here we describe a role for KDEL receptor 1 (KDELR1) that involves the regulation of integrated stress responses (ISR) in T cells. Designing and using an N-ethyl-N-nitrosourea (ENU)-mutant mouse line, T-Red (naïve T-cell reduced), we show that a point mutation in KDELR1 is responsible for the reduction in the number of naïve T cells in this model owing to an increase in ISR. Mechanistic analysis shows that KDELR1 directly regulates protein phosphatase 1 (PP1), a key phosphatase for ISR in naïve T cells. T-Red KDELR1 does not associate with PP1, resulting in reduced phosphatase activity against eIF2α and subsequent expression of stress responsive genes including the proapoptotic factor Bim. These results demonstrate that KDELR1 regulates naïve T-cell homeostasis by controlling ISR.

Suggested Citation

  • Daisuke Kamimura & Kokichi Katsunuma & Yasunobu Arima & Toru Atsumi & Jing-jing Jiang & Hidenori Bando & Jie Meng & Lavannya Sabharwal & Andrea Stofkova & Naoki Nishikawa & Hironao Suzuki & Hideki Ogu, 2015. "KDEL receptor 1 regulates T-cell homeostasis via PP1 that is a key phosphatase for ISR," Nature Communications, Nature, vol. 6(1), pages 1-14, November.
  • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8474
    DOI: 10.1038/ncomms8474
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms8474
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/ncomms8474?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms8474. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.