Int. J. Dev. Biol. 59: 281 - 288 (2015)

https://doi.org/10.1387/ijdb.150196lr

Vol 59, Issue 7-8-9

Special Issue: Ionic Messengers in Development and Cancer

TRPM channels and magnesium in early embryonic development

Published: 19 November 2015

Yuko Komiya* and Loren W. Runnels*

Department of Pharmacology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, USA

Abstract

Magnesium (Mg²⁺) is the second most abundant cellular cation and is essential for all stages of life, from the early embryo to adult. Mg²⁺ deficiency causes or contributes to many human diseases, including migraine headaches, Parkinson’s disease, Alzheimer’s disease, hypotension, type 2 diabetes mellitus and cardiac arrhythmias. Although the concentration of Mg²⁺ in the extracellular environment can vary significantly, the total intracellular Mg²⁺ concentration is actively maintained within a relatively narrow range (14 – 20 mM) via tight, yet poorly understood, regulation of intracellular Mg²⁺ by Mg²⁺ transporters and Mg²⁺-permeant ion channels. Recent studies have continued to add to the growing number of Mg²⁺ transporters and ion channels involved in Mg²⁺ homeostasis, including TRPM6 and TRPM7, members of the transient receptor potential (TRP) ion channel family. Mutations in TRPM6, including amino acid substitutions that prevent its heterooligomerization with TRPM7, occur in the rare autosomal-recessive disease hypomagnesemia with secondary hypocalcemia (HSH). Genetic ablation of either gene in mice results in early embryonic lethality, raising the question of whether these channels’ capacity to mediate Mg²⁺ influx plays an important role in embryonic development. Here we review what is known of the function of Mg²⁺ in early development and summarize recent findings regarding the function of the TRPM6 and TRPM7 ion channels during embryogenesis.

Keywords

magnesium, TRPM7, TRPM6, ion channel, gastrulation, embryonic development