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EBSCOhost Psychology and Behavioral Sciences Collection
Beschreibungen/Notizen
The parathyroid glands are the only known source of circulating parathyroid
hormone (PTH), which initiates an endocrine cascade that regulates serum calcium
concentration. Glial cells missing2 (Gcm2), a
mouse homologue of Drosophila Gcm, is the only transcription
factor whose expression is restricted to the parathyroid glands.
Here we show that Gcm2-deficient mice lack parathyroid glands and exhibit
a biological hypoparathyroidism, identifying Gcm2 as a master regulatory
gene of parathyroid gland development. Unlike PTH receptor-deficient
mice, however, Gcm2-deficient mice are viable and fertile, and have
only a mildly abnormal bone phenotype. Despite their lack of parathyroid glands,
Gcm2-deficient mice have PTH serum levels identical to those of wild-type
mice, as do parathyroidectomized wild-type animals. Expression and ablation
studies identified the thymus, where Gcm1, another Gcm homologue, is
expressed, as the additional, downregulatable source of PTH. Thus, Gcm2
deletion uncovers an auxiliary mechanism for the regulation of calcium
homeostasis in the absence of parathyroid glands. We propose that this backup
mechanism may be a general feature of endocrine regulation.