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Abstract

Normal reproductive function in InhBP/p120-deficient mice (HTML) 
Bernard,Daniel J.; Burns,Kathleen H.; Haupt,Bisong; Matzuk,Martin M.; Woodruff,Teresa K.
Molecular and Cellular Biology 23(14): 4882-4891
Publication date: 2003

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The inhibins are gonadal transforming growth factor ßsuperfamily protein hormones that suppress pituitary follicle-stimulatinghormone (FSH) synthesis. Recently, betaglycan and inhibin bindingprotein (InhBP/p120, also known as the product of immunoglobulinsuperfamily gene 1 [IGSF1]) were identified as candidate inhibincoreceptors, shedding light on the molecular basis of how inhibinsmay affect target cells. Activins, which are structurally relatedto the inhibins, act within the pituitary to stimulate FSH production.Betaglycan increases the affinity of inhibins for the activintype IIA (ACVR2) receptor, thereby blocking activin bindingand signaling through this receptor. InhBP/p120 may not directlybind inhibins but may interact with the activin type IB receptor,ALK4, and participate in inhibin B's antagonism of activin signaling.To better understand the in vivo functions of InhBP/p120, wecharacterized the InhBP/p120 mRNAs and gene in mice and generatedInhBP/p120 mutant mice by gene targeting in embryonic stem cells.InhBP/p120 mutant male and female mice were viable and fertile.Moreover, they showed no alterations in FSH synthesis or secretionor in ovarian or testicular function. These data contributeto a growing body of evidence indicating that InhBP/p120 doesnot play an essential role in inhibin biology.

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