Deletion of Trpm7 disrupts embryonic development and thymopoiesis without altering Mg2+ homeostasis.

Published

Journal Article

The gene transient receptor potential-melastatin-like 7 (Trpm7) encodes a protein that functions as an ion channel and a kinase. TRPM7 has been proposed to be required for cellular Mg2+ homeostasis in vertebrates. Deletion of mouse Trpm7 revealed that it is essential for embryonic development. Tissue-specific deletion of Trpm7 in the T cell lineage disrupted thymopoiesis, which led to a developmental block of thymocytes at the double-negative stage and a progressive depletion of thymic medullary cells. However, deletion of Trpm7 in T cells did not affect acute uptake of Mg2+ or the maintenance of total cellular Mg2+. Trpm7-deficient thymocytes exhibited dysregulated synthesis of many growth factors that are necessary for the differentiation and maintenance of thymic epithelial cells. The thymic medullary cells lost signal transducer and activator of transcription 3 activity, which accounts for their depletion when Trpm7 is disrupted in thymocytes.

Full Text

Duke Authors

Cited Authors

  • Jin, J; Desai, BN; Navarro, B; Donovan, A; Andrews, NC; Clapham, DE

Published Date

  • October 31, 2008

Published In

Volume / Issue

  • 322 / 5902

Start / End Page

  • 756 - 760

PubMed ID

  • 18974357

Pubmed Central ID

  • 18974357

Electronic International Standard Serial Number (EISSN)

  • 1095-9203

Digital Object Identifier (DOI)

  • 10.1126/science.1163493

Language

  • eng

Conference Location

  • United States