TRPM6 and TRPM7: Novel players in cell intercalation during vertebrate embryonic development

Dev Dyn. 2020 Aug;249(8):912-923. doi: 10.1002/dvdy.182. Epub 2020 May 26.

Abstract

A common theme in organogenesis is how the final structure of organs emerge from epithelial tube structures, with the formation of the neural tube being one of the best examples. Two types of cell movements co-occur during neural tube closure involving the migration of cells toward the midline of the embryo (mediolateral intercalation or convergent extension) as well as the deep movement of cells from inside the embryo to the outside of the lateral side of the neural plate (radial intercalation). Failure of either type of cell movement will prevent neural tube closure, which can produce a range of neural tube defects (NTDs), a common congenital disease in humans. Numerous studies have identified signaling pathways that regulate mediolateral intercalation during neural tube closure. Less understood are the pathways that govern radial intercalation. Using the Xenopus laevis system, our group reported the identification of transient receptor potential (TRP) channels, TRPM6 and TRPM7, and the Mg2+ ion they conduct, as novel and key factors regulating both mediolateral and radial intercalation during neural tube closure. Here we broadly discuss tubulogenesis and cell intercalation from the perspective of neural tube closure and the respective roles of TRPM7 and TRPM6 in this critical embryonic process.

Keywords: TRPM6; TRPM7; Xenopus; cell intercalation; magnesium; neural tube closure.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • 3T3 Cells
  • Animals
  • Cell Movement
  • Embryonic Development
  • Gene Expression Regulation, Developmental*
  • Humans
  • Ions
  • Magnesium / chemistry*
  • Magnesium / metabolism
  • Mice
  • Neural Plate / metabolism
  • Neural Tube / metabolism
  • Neural Tube Defects / genetics
  • Neural Tube Defects / metabolism
  • Neurulation
  • Protein Domains
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / physiology*
  • Signal Transduction
  • TRPM Cation Channels / genetics
  • TRPM Cation Channels / metabolism
  • TRPM Cation Channels / physiology*
  • Xenopus Proteins / genetics
  • Xenopus Proteins / physiology*
  • Xenopus laevis / metabolism*
  • Zebrafish

Substances

  • Ions
  • TRPM Cation Channels
  • TRPM6 protein, human
  • TRPM7 protein, Xenopus
  • Trpm6 protein, mouse
  • Xenopus Proteins
  • Trpm7 protein, mouse
  • Protein Serine-Threonine Kinases
  • TRPM7 protein, human
  • Magnesium