ZFIN ID: ZDB-PUB-180225-2
Microbiota promote secretory cell determination in the intestinal epithelium by modulating host Notch signaling
Troll, J.V., Hamilton, M.K., Abel, M.L., Ganz, J., Bates, J.M., Stephens, W.Z., Melancon, E., van der Vaart, M., Meijer, A.H., Distel, M., Eisen, J.S., Guillemin, K.
Date: 2018
Source: Development (Cambridge, England)   145(4): (Journal)
Registered Authors: Bates, Jennifer M., Distel, Martin, Eisen, Judith S., Ganz, Julia, Guillemin, Karen, Meijer, Annemarie H., Stephen, W. Zac, van der Vaart, Michiel
Keywords: Intestinal cell determination, Microbiota, Myd88, Notch, Secretory cell, Zebrafish
MeSH Terms:
  • Animals
  • Intestinal Mucosa/metabolism*
  • Intestinal Mucosa/microbiology
  • Intestinal Mucosa/physiology
  • Microbiota*
  • Myeloid Differentiation Factor 88/metabolism*
  • Receptors, Notch/metabolism*
  • Signal Transduction/physiology
  • Zebrafish/metabolism
PubMed: 29475973 Full text @ Development
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ABSTRACT
Resident microbes promote many aspects of host development, although the mechanisms by which microbiota influence host tissues remain unclear. We showed previously that the microbiota is required for allocation of appropriate numbers of secretory cells in the zebrafish intestinal epithelium. Because Notch signaling is crucial for secretory fate determination, we conducted epistasis experiments to establish whether the microbiota modulates host Notch signaling. We also investigated whether innate immune signaling transduces microbiota cues via the Myd88 adaptor protein. We provide the first evidence that microbiota-induced, Myd88-dependent signaling inhibits host Notch signaling in the intestinal epithelium, thereby promoting secretory cell fate determination. These results connect microbiota activity via innate immune signaling to the Notch pathway, which also plays crucial roles in intestinal homeostasis throughout life and when impaired can result in chronic inflammation and cancer.
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