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

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. Moresco, John R. Yates, Parastoo Azadi, Josephine Ni, George M. H. Birchenough, Bruce Beutler and Emre E. Turer ()
Additional contact information
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
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
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

Nature Communications, 2023, vol. 14, issue 1, 1-13

Abstract: 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.

Date: 2023
References: View references in EconPapers View complete reference list from CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-023-39398-1 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-39398-1

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-39398-1

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().