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Trans-Golgi protein TVP23B regulates host-microbe interactions via Paneth cell homeostasis and Goblet cell glycosylation

Author

Listed:
  • Ran Song

    (University of Texas Southwestern Medical Center)

  • William McAlpine

    (University of Texas Southwestern Medical Center)

  • Aaron M. Fond

    (University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center)

  • Evan Nair-Gill

    (University of Texas Southwestern Medical Center)

  • Jin Huk Choi

    (University of Texas Southwestern Medical Center)

  • Elisabeth E. L. Nyström

    (University of Kiel)

  • Liisa Arike

    (University of Gothenburg)

  • Sydney Field

    (University of Texas Southwestern Medical Center)

  • Xiaohong Li

    (University of Texas Southwestern Medical Center)

  • Jeffrey A. SoRelle

    (University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center)

  • James J. Moresco

    (University of Texas Southwestern Medical Center)

  • Eva Marie Y. Moresco

    (University of Texas Southwestern Medical Center)

  • John R. Yates

    (The Scripps Research Institute)

  • Parastoo Azadi

    (University of Georgia)

  • Josephine Ni

    (University of Texas Southwestern Medical Center)

  • George M. H. Birchenough

    (University of Gothenburg)

  • Bruce Beutler

    (University of Texas Southwestern Medical Center)

  • Emre E. Turer

    (University of Texas Southwestern Medical Center
    University of Texas Southwestern Medical Center)

Abstract

A key feature in intestinal immunity is the dynamic intestinal barrier, which separates the host from resident and pathogenic microbiota through a mucus gel impregnated with antimicrobial peptides. Using a forward genetic screen, we have found a mutation in Tvp23b, which conferred susceptibility to chemically induced and infectious colitis. Trans-Golgi apparatus membrane protein TVP23 homolog B (TVP23B) is a transmembrane protein conserved from yeast to humans. We found that TVP23B controls the homeostasis of Paneth cells and function of goblet cells, leading to a decrease in antimicrobial peptides and more penetrable mucus layer. TVP23B binds with another Golgi protein, YIPF6, which is similarly critical for intestinal homeostasis. The Golgi proteomes of YIPF6 and TVP23B-deficient colonocytes have a common deficiency of several critical glycosylation enzymes. TVP23B is necessary for the formation of the sterile mucin layer of the intestine and its absence disturbs the balance of host and microbe in vivo.

Suggested Citation

  • Ran Song & William McAlpine & Aaron M. Fond & Evan Nair-Gill & Jin Huk Choi & Elisabeth E. L. Nyström & Liisa Arike & Sydney Field & Xiaohong Li & Jeffrey A. SoRelle & James J. Moresco & Eva Marie Y. , 2023. "Trans-Golgi protein TVP23B regulates host-microbe interactions via Paneth cell homeostasis and Goblet cell glycosylation," Nature Communications, Nature, vol. 14(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-39398-1
    DOI: 10.1038/s41467-023-39398-1
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    References listed on IDEAS

    as
    1. Timon E. Adolph & Michal F. Tomczak & Lukas Niederreiter & Hyun-Jeong Ko & Janne Böck & Eduardo Martinez-Naves & Jonathan N. Glickman & Markus Tschurtschenthaler & John Hartwig & Shuhei Hosomi & Magda, 2013. "Paneth cells as a site of origin for intestinal inflammation," Nature, Nature, vol. 503(7475), pages 272-276, November.
    2. Tao Wang & Chun Hui Bu & Sara Hildebrand & Gaoxiang Jia & Owen M. Siggs & Stephen Lyon & David Pratt & Lindsay Scott & Jamie Russell & Sara Ludwig & Anne R. Murray & Eva Marie Y. Moresco & Bruce Beutl, 2018. "Probability of phenotypically detectable protein damage by ENU-induced mutations in the Mutagenetix database," Nature Communications, Nature, vol. 9(1), pages 1-10, December.
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    Cited by:

    1. Xue Zhong & Nagesh Peddada & Jianhui Wang & James J. Moresco & Xiaowei Zhan & John M. Shelton & Jeffrey A. SoRelle & Katie Keller & Danielle Renee Lazaro & Eva Marie Y. Moresco & Jin Huk Choi & Bruce , 2023. "OVOL2 sustains postnatal thymic epithelial cell identity," Nature Communications, Nature, vol. 14(1), pages 1-22, December.

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