IPMK and β-catenin mediate PLC-β1-dependent signaling in myogenic differentiation
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Giulia Ramazzotti1, Anna Maria Billi1, Lucia Manzoli1, Cristina Mazzetti1, Alessandra Ruggeri1, Christophe Erneux2, Seyun Kim4, Pann-Ghill Suh3, Lucio Cocco1, Irene Faenza1
1Cellular Signalling Laboratory, Department of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy
2Interdisciplinary Research Institute (IRIBHM), Université Libre de Bruxelles, Campus Erasme, Brussels, Belgium
3Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea
4Department of Biological Sciences, KAIST, Daejeon, Republic of Korea
Lucio Cocco, email: [email protected]
Irene Faenza, email: [email protected]
Keywords: myogenic differentiation, phospholipase C-β1, IPMK, β-catenin, inositol phosphates
Received: June 06, 2016 Accepted: August 15, 2016 Published: August 23, 2016
In previous studies, we have reported that phospholipase C (PLC)-β1 plays a crucial role in myogenic differentiation and we determined the importance of its catalytic activity for the initiation of this process. Here we define the effectors that take part to its signaling pathway. We show that the Inositol Polyphosphate Multikinase (IPMK) is able to promote myogenic differentiation since its overexpression determines the up-regulation of several myogenic markers. Moreover, we demonstrate that IPMK activates the same cyclin D3 promoter region targeted by PLC-β1 and that IPMK-induced promoter activation relies upon c-jun binding to the promoter, as we have shown previously for PLC-β1. Furthermore, our data shows that IPMK overexpression causes an increase in β-catenin translocation and accumulation to the nuclei of differentiating myoblasts resulting in higher MyoD activation. Finally, we describe that PLC-β1 overexpression determines too an increase in β-catenin translocation and that PLC-β1, IPMK and β-catenin are mediators of the same signaling pathway since their overexpression results in cyclin D3 and myosin heavy chain (MYH) induction.
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