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Am J Physiol Renal Physiol 278: F507-F514, 2000;
0363-6127/00 $5.00
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Vol. 278, Issue 4, F507-F514, April 2000

INVITED REVIEW
Variable imprinting of the heterotrimeric G protein Gs alpha -subunit within different segments of the nephron

Lee S. Weinstein1, Shuhua Yu1, and Carolyn A. Ecelbarger2

1 Metabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; and 2 Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, District of Columbia 20007

The heterotrimeric G protein Gs is required for hormone-stimulated intracellular cAMP generation because it couples hormone receptors to the enzyme adenylyl cyclase. Hormones that activate Gs in the kidney include parathyroid hormone, glucagon, calcitonin, and vasopressin. Recently, it has been demonstrated that the Gsalpha gene is imprinted in a tissue-specific manner, leading to preferential expression of Gsalpha from the maternal allele in some tissues. In the kidney, Gsalpha is imprinted in the proximal tubule but not in more distal nephron segments, such as the thick ascending limb or collecting duct. This most likely explains why in both humans and mice heterozygous mutations in the maternal allele lead to parathyroid hormone resistance in the proximal tubule whereas mutations in the paternal allele do not. In contrast, heterozygous mutations have little effect on vasopressin action in the collecting ducts. In mice with heterozygous null Gsalpha mutations (both those with mutations on the maternal or paternal allele), expression of the Na-K-2Cl cotransporter was decreased in the thick ascending limb, suggesting that its expression is regulated by cAMP. The Gsalpha genes also generate alternative, oppositely imprinted transcripts encoding XLalpha s, a Gsalpha isoform with a long NH2-terminal extension, and NESP55, a chromogranin-like neurosecretory protein. The role, if any, of these proteins in renal physiology is unknown.

genomic imprinting; Albright hereditary osteodystrophy; adenosine 3',5'-cyclic monophosphate; pseudohypoparathyroidism; parathyroid hormone


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