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

Julie Batut | Zendy; Bernhard Schmierer | Zendy; Jing Cao | Zendy; Laurel A. Raftery | Zendy; Caroline S. Hill | Zendy; Michael Howell | Zendy

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

Author(s) -

Julie Batut,

Bernhard Schmierer,

Jing Cao,

Laurel A. Raftery,

Caroline S. Hill,

Michael Howell

Publication year - 2008

Publication title -

development

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.754

H-Index - 325

eISSN - 1477-9129

pISSN - 0950-1991

DOI - 10.1242/dev.020842

Subject(s) - biology , nodal , nodal signaling , activin receptor , activin type 2 receptors , microbiology and biotechnology , signalling , tgf beta signaling pathway , transforming growth factor , protein phosphatase 2 , protein subunit , acvr2b , transforming growth factor beta , smad2 protein , endocrinology , medicine , cancer research , gene , anatomy , genetics , embryogenesis , embryo , gastrulation

We identify Balpha (PPP2R2A) and Bdelta (PPP2R2D), two highly related members of the B family of regulatory subunits of the protein phosphatase PP2A, as important modulators of TGF-beta/Activin/Nodal signalling that affect the pathway in opposite ways. Knockdown of Balpha in Xenopus embryos or mammalian tissue culture cells suppresses TGF-beta/Activin/Nodal-dependent responses, whereas knockdown of Bdelta enhances these responses. Moreover, in Drosophila, overexpression of Smad2 rescues a severe wing phenotype caused by overexpression of the single Drosophila PP2A B subunit Twins. We show that, in vertebrates, Balpha enhances TGF-beta/Activin/Nodal signalling by stabilising the basal levels of type I receptor, whereas Bdelta negatively modulates these pathways by restricting receptor activity. Thus, these highly related members of the same subfamily of PP2A regulatory subunits differentially regulate TGF-beta/Activin/Nodal signalling to elicit opposing biological outcomes.

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