作者: Thomas Günther , Zhou-Feng Chen , Jaesang Kim , Matthias Priemel , Johannes M. Rueger
DOI: 10.1038/35018111
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摘要: The parathyroid glands are the only known source of circulating hormone (PTH), which initiates an endocrine cascade that regulates serum calcium concentration. Glial cells missing (Gcm2), a mouse homologue Drosophila Gcm, is transcription factor whose expression restricted to glands. Here we show Gcm2-deficient mice lack and exhibit biological hypoparathyroidism, identifying Gcm2 as master regulatory gene gland development. Unlike PTH receptor-deficient mice, however, viable fertile, have mildly abnormal bone phenotype. Despite their glands, levels identical those wild-type do parathyroidectomized animals. Expression ablation studies identified thymus, where Gcm1, another Gcm homologue, expressed, additional, downregulatable PTH. Thus, deletion uncovers auxiliary mechanism for regulation homeostasis in absence We propose this backup may be general feature regulation.