Generation of mice encoding a conditional null allele of Gcm2

Ziqiang Yuan, Evan E. Opas, Chakravarthy Vrikshajanani, Steven K. Libutti, Michael A. Levine

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

Glial cells missing homolog 2 (GCM2) is a transcription factor that is expressed predominately in the pharyngeal pouches and, at later stages, in the developing and mature parathyroid glands. In humans, loss of GCM2 function, either through recessive apomorphic mutations or dominant inhibitor mutations in the human GCM2 gene, leads to isolated hypoparathyroidism. In mice, homozygous disruption of Gcm2 by conventional gene targeting results in parathyroid aplasia and hypoparathyroidism. In this study, we report the generation and functional characterization of mice encoding a conditional null allele of Gcm2. We demonstrate the functional integrity of the conditional Gcm2 allele and report successful in vivo deletion of exon 2 using Cre recombinase. The mice with conditional deletion of Gcm2 displayed phenotypes similar to those previously described for a conventional Gcm2 knockout, including perinatal lethality, hypocalemia, low or undetectable serum levels of parathyroid hormone, and absent parathyroid glands. The production of a conditional mutant allele for Gcm2 represents a valuable resource for the study of the temporal- and spatial-specific roles for Gcm2, and for understanding the postnatal activities of GCM2 protein.

Original languageEnglish (US)
Pages (from-to)631-641
Number of pages11
JournalTransgenic Research
Volume23
Issue number4
DOIs
StatePublished - Aug 2014

Keywords

  • Gcm2
  • Knockout mice
  • Parathyroid gland
  • Parathyroid hormone

ASJC Scopus subject areas

  • Biotechnology
  • Animal Science and Zoology
  • Agronomy and Crop Science
  • Genetics

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  • Cite this

    Yuan, Z., Opas, E. E., Vrikshajanani, C., Libutti, S. K., & Levine, M. A. (2014). Generation of mice encoding a conditional null allele of Gcm2. Transgenic Research, 23(4), 631-641. https://doi.org/10.1007/s11248-014-9799-7