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First published online August 12, 2008

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New regulatory twist to TGF-β signalling

TGF-β/Activin/Nodal signalling regulates many developmental processes and is itself regulated in a highly complex fashion. Now, Batut and co-workers unexpectedly reveal that two closely related regulatory subunits of the serine/threonine protein phosphatase PP2A - B and B - modulate TGF-β/Activin/Nodal signalling in opposite ways (see p. 2927). TGF-β/Activin/Nodal ligands bind to type II serine/threonine receptor kinases, which phosphorylate and activate type I receptor kinases. These phosphorylate receptor-regulated Smads, which form complexes with Smad4 that affect development by regulating target gene expression. The researchers show that B knockdown in Xenopus embryos and in mammalian cells in culture suppresses TGF-β/Activin/Nodal-dependent responses, but that B knockdown enhances these responses. Other experiments indicate that B enhances TGF-β/Activin/Nodal signalling by stabilizing type I receptor basal levels, whereas B reduces signalling by restricting receptor activity. Thus, suggest the researchers, the ratio of B to B in a cell will influence its threshold response to TGF-β/Activin/Nodal ligands and consequently determine its subsequent behaviour.

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Related articles in Development:

Two highly related regulatory subunits of PP2A exert opposite effects on TGF-β/Activin/Nodal signalling

Julie Batut, Bernhard Schmierer, Jing Cao, Laurel A. Raftery, Caroline S. Hill, and Michael Howell
Development 2008 135: 2927-2937. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?