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Related Experiment Video

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Mouse Fetal Whole Intestine Culture System for Ex Vivo Manipulation of Signaling Pathways and Three-dimensional Live Imaging of Villus Development
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TMEM132A regulates mouse hindgut morphogenesis and caudal development.

Huiqing Zeng1, Aimin Liu1

  • 1Department of Biology, Eberly College of Science and Huck Institute of Life Sciences, The Pennsylvania State University, University Park, PA 16802, USA.

Development (Cambridge, England)
|June 30, 2023
PubMed
Summary

Transmembrane protein 132a (Tmem132a) regulates hindgut development, preventing caudal developmental defects. Tmem132a mutations cause hindgut malformations, leading to defects in multiple caudal structures.

Keywords:
Caudal regressionCloacaConvergent extensionDefinitive endodermMousePlanar cell polaritySirenomeliaSpina bifidaVisceral endoderm

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Caudal developmental defects impact multiple organ systems.
  • Previous research implicated mesodermal migration and blood supply issues, but these don't fully explain all defects.

Purpose of the Study:

  • To investigate the role of Transmembrane protein 132a (Tmem132a) in caudal development.
  • To identify the underlying mechanisms of caudal developmental defects in Tmem132a mutant mice.

Main Methods:

  • Generation and analysis of Tmem132a mutant mice.
  • Histological examination of embryonic development.
  • Molecular analysis of gene interactions and protein localization.

Main Results:

  • Tmem132a mutant embryos exhibit skeletal, neural tube closure, genitourinary, and hindgut defects.
  • Visceral endoderm fails to be excluded from the early hindgut in Tmem132a mutants.
  • TMEM132A interacts with Planar Cell Polarity (PCP) pathway components CELSR1 and FZD6.
  • Tmem132a acts synergistically with Vangl2 in neural tube closure.

Conclusions:

  • Tmem132a is a novel regulator of PCP and hindgut development.
  • Hindgut malformation is the primary cause of diverse caudal developmental defects in Tmem132a mutants.