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TMBIM4 affects left-right patterning via pluripotency exit during gastrulation.

Nicholas S Diab1, Valentyna Kostiuk1, Leonid Tyan2

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Transmembrane BAX inhibitor motif-containing protein 4 (TMBIM4) is crucial for left-right patterning in embryonic development. Its depletion causes congenital heart defects by disrupting gastrulation and cell fate, highlighting TMBIM4 as a potential CHD gene.

Keywords:
Congenital heart diseaseElectrophysiologyEmbryonic developmentXenopus tropicalision channels

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Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • Congenital heart disease (CHD) is the most common birth defect, yet its genetic underpinnings are not fully understood.
  • Transmembrane BAX inhibitor motif-containing protein 4 (TMBIM4) is a candidate gene for CHD, linked to left-right (LR) patterning defects like cardiac heterotaxy.
  • The precise developmental role of TMBIM4, particularly in early embryogenesis and cardiac development, requires further investigation.

Purpose of the Study:

  • To investigate the developmental function of tmbim4 in Xenopus tropicalis.
  • To determine tmbim4's role in left-right (LR) patterning and cardiac asymmetry.
  • To elucidate the molecular mechanisms by which TMBIM4 influences embryonic development and cell fate.

Main Methods:

  • Depletion of tmbim4 in Xenopus tropicalis embryos.
  • Assessment of cardiac asymmetry and LR patterning defects.
  • Analysis of gastrulation, pluripotency marker expression, and cell membrane potential (Vm).
  • Rescue experiments using human and viral TMBIM4 orthologs and choline application.

Main Results:

  • tmbim4 depletion in Xenopus caused cardiac asymmetry defects, mirroring human CHD phenotypes.
  • Gastrulation was impaired in tmbim4-depleted embryos, affecting pluripotency marker expression and exit.
  • tmbim4 depletion led to embryo depolarization, which was rescued by choline, suggesting an ion channel function.
  • Evidence suggests TMBIM4 localizes to the plasma membrane, potentially regulating Vm.

Conclusions:

  • tmbim4 is essential for proper LR patterning and gastrulation during embryonic development.
  • TMBIM4 functions as a putative ion channel, influencing cell membrane potential and cell fate.
  • These findings establish tmbim4 as a plausible gene associated with congenital heart disease and provide novel insights into its developmental roles.