Functional Effects of PTPN11 (SHP2) Mutations Causing LEOPARD Syndrome on Epidermal Growth Factor-Induced Phosphoinositide 3-Kinase/AKT/Glycogen Synthase Kinase 3β Signaling

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Published inMolecular and Cellular Biology Vol. 30; no. 10; pp. 2498 - 2507
Main Authors Serra-Nedelec, A., Treguer, K., Tajan, M., Araki, T., Dance, M., Mus, M., Montagner, A., Valet, P., Neel, B., Edouard, Thomas, Combier, Jean-Philippe, Nédélec, Audrey, Bel-Vialar, Sophie, Métrich, Mélanie, Conte-Auriol, Francoise, Lyonnet, Stanislas, Parfait, Béatrice, Tauber, Maithé, Salles, Jean-Pierre, Lezoualc'H, Frank, Yart, Armelle, Raynal, Patrick
Format Journal Article
LanguageEnglish
Published American Society for Microbiology 15.05.2010
Taylor & Francis
American Society for Microbiology (ASM)
Subjects
Life Sciences
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList LEOPARD syndrome (LS), a disorder with multiple developmental abnormalities, is mainly due to mutations that impair the activity of the tyrosine phosphatase SHP2 (PTPN11). How these alterations cause the disease remains unknown. We report here that fibroblasts isolated from LS patients displayed stronger epidermal growth factor (EGF)-induced phosphorylation of both AKT and glycogen synthase kinase 3β (GSK-3β) than fibroblasts from control patients. Similar results were obtained in HEK293 cells expressing LS mutants of SHP2. We found that the GAB1/phosphoinositide 3-kinase (PI3K) complex was more abundant in fibroblasts from LS than control subjects and that both AKT and GSK-3β hyperphosphorylation were prevented by reducing GAB1 expression or by overexpressing a GAB1 mutant unable to bind to PI3K. Consistently, purified recombinant LS mutants failed to dephosphorylate GAB1 PI3K-binding sites. These mutants induced PI3K-dependent increase in cell size in a model of chicken embryo cardiac explants and in transcriptional activity of the atrial natriuretic factor (ANF) gene in neonate rat cardiomyocytes. In conclusion, SHP2 mutations causing LS facilitate EGF-induced PI3K/AKT/GSK-3β stimulation through impaired GAB1 dephosphorylation, resulting in deregulation of a novel signaling pathway that could be involved in LS pathology.
LEOPARD syndrome (LS), a disorder with multiple developmental abnormalities, is mainly due to mutations that impair the activity of the tyrosine phosphatase SHP2 ( PTPN11 ). How these alterations cause the disease remains unknown. We report here that fibroblasts isolated from LS patients displayed stronger epidermal growth factor (EGF)-induced phosphorylation of both AKT and glycogen synthase kinase 3β (GSK-3β) than fibroblasts from control patients. Similar results were obtained in HEK293 cells expressing LS mutants of SHP2. We found that the GAB1/phosphoinositide 3-kinase (PI3K) complex was more abundant in fibroblasts from LS than control subjects and that both AKT and GSK-3β hyperphosphorylation were prevented by reducing GAB1 expression or by overexpressing a GAB1 mutant unable to bind to PI3K. Consistently, purified recombinant LS mutants failed to dephosphorylate GAB1 PI3K-binding sites. These mutants induced PI3K-dependent increase in cell size in a model of chicken embryo cardiac explants and in transcriptional activity of the atrial natriuretic factor (ANF) gene in neonate rat cardiomyocytes. In conclusion, SHP2 mutations causing LS facilitate EGF-induced PI3K/AKT/GSK-3β stimulation through impaired GAB1 dephosphorylation, resulting in deregulation of a novel signaling pathway that could be involved in LS pathology.
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Author Béatrice Parfait
Mélanie Métrich
Jean-Pierre Salles
Frank Lezoualc'h
Francoise Conte-Auriol
Stanislas Lyonnet
Patrick Raynal
Sophie Bel-Vialar
Audrey Nédélec
Armelle Yart
Thomas Edouard
Jean-Philippe Combier
Maithé Tauber
AuthorAffiliation INSERM U563, Centre de Physiopathologie de Toulouse-Purpan, F-31024 Toulouse, France, 1 CHRU and Université Toulouse III, Hôpital Purpan, F-31059 Toulouse, France, 2 Centre de Biologie du Développement, CNRS UMR5547, F-31062 Toulouse, France, 3 INSERM UMRS 769, Signalisation et Physiopathologie Cardiaque, Université Paris Sud 11, F-92296 Châtenay-Malabry, France, 4 Université Paris Descartes and INSERM U781, Hôpital Necker, F-75743 Paris, France, 5 Université Paris Descartes and INSERM U745, UFR Pharmacie, F-75270 Paris, France 6
AuthorAffiliation_xml – name: INSERM U563, Centre de Physiopathologie de Toulouse-Purpan, F-31024 Toulouse, France, 1 CHRU and Université Toulouse III, Hôpital Purpan, F-31059 Toulouse, France, 2 Centre de Biologie du Développement, CNRS UMR5547, F-31062 Toulouse, France, 3 INSERM UMRS 769, Signalisation et Physiopathologie Cardiaque, Université Paris Sud 11, F-92296 Châtenay-Malabry, France, 4 Université Paris Descartes and INSERM U781, Hôpital Necker, F-75743 Paris, France, 5 Université Paris Descartes and INSERM U745, UFR Pharmacie, F-75270 Paris, France 6
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T.E. and J.-P.C. contributed equally to the work.
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LEOPARD syndrome (LS), a disorder with multiple developmental abnormalities, is mainly due to mutations that impair the activity of the tyrosine phosphatase...
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SubjectTerms Life Sciences
Title Functional Effects of PTPN11 (SHP2) Mutations Causing LEOPARD Syndrome on Epidermal Growth Factor-Induced Phosphoinositide 3-Kinase/AKT/Glycogen Synthase Kinase 3β Signaling
URI http://mcb.asm.org/content/30/10/2498.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.00646-09
https://hal.science/hal-03191859
https://pubmed.ncbi.nlm.nih.gov/PMC2863708
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