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N-cadherin activation substitutes for the cell contact control in cell cycle arrest and myogenic differentiation: involvement of p120 and beta-catenin.
J Biol Chem 2004; 279(35):36795-802JB

Abstract

N-cadherin is expressed throughout skeletal myogenesis and has been proposed to be involved in the differentiation program of myogenic precursors. Here, we further characterize the N-cadherin involvement and its mechanism of action at the onset of differentiation, through controlled N-cadherin activation by plating isolated C2 myoblasts on surfaces coated with a chimeric Ncad-Fc homophilic ligand (N-cadherin ectodomain fused to the immunoglobulin G Fc fragment). We show that N-cadherin activation substitutes for the cell density in myogenic differentiation by promoting myogenin and troponin T expression. In addition, N-cadherin adhesion participates to the associated cell cycle arrest through the nuclear accumulation of cyclin-dependent kinase inhibitors p21 and p27. Mouse primary myoblast cultures exhibited similar responses to N-cadherin as C2 cells. RNA interference knockdowns of the N-cadherin-associated cytoplasmic proteins p120 and beta-catenin produced opposite effects on the differentiation pathway. p120 silencing resulted in a decreased myogenic differentiation, associated with a reduction in cadherin-catenin content, which may explain its action on myogenic differentiation. beta-Catenin silencing led to a stimulatory effect on myogenin expression, without any effect on cell cycle. Our results demonstrate that N-cadherin adhesion may account for cell-cell contact-dependent cell cycle arrest and differentiation of myogenic cells, involving regulation through p120 and beta-catenins.

Authors+Show Affiliations

Signalisation et Différenciation Cellulaires dans les Systèmes Nerveux et Musculaire, U440 INSERM/UPMC, Institut du Fer à Moulin, 17 rue du Fer à Moulin, 75005 Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15194693

Citation

Gavard, Julie, et al. "N-cadherin Activation Substitutes for the Cell Contact Control in Cell Cycle Arrest and Myogenic Differentiation: Involvement of P120 and Beta-catenin." The Journal of Biological Chemistry, vol. 279, no. 35, 2004, pp. 36795-802.
Gavard J, Marthiens V, Monnet C, et al. N-cadherin activation substitutes for the cell contact control in cell cycle arrest and myogenic differentiation: involvement of p120 and beta-catenin. J Biol Chem. 2004;279(35):36795-802.
Gavard, J., Marthiens, V., Monnet, C., Lambert, M., & Mège, R. M. (2004). N-cadherin activation substitutes for the cell contact control in cell cycle arrest and myogenic differentiation: involvement of p120 and beta-catenin. The Journal of Biological Chemistry, 279(35), pp. 36795-802.
Gavard J, et al. N-cadherin Activation Substitutes for the Cell Contact Control in Cell Cycle Arrest and Myogenic Differentiation: Involvement of P120 and Beta-catenin. J Biol Chem. 2004 Aug 27;279(35):36795-802. PubMed PMID: 15194693.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-cadherin activation substitutes for the cell contact control in cell cycle arrest and myogenic differentiation: involvement of p120 and beta-catenin. AU - Gavard,Julie, AU - Marthiens,Véronique, AU - Monnet,Céline, AU - Lambert,Mireille, AU - Mège,René Marc, Y1 - 2004/06/11/ PY - 2004/6/15/pubmed PY - 2004/10/7/medline PY - 2004/6/15/entrez SP - 36795 EP - 802 JF - The Journal of biological chemistry JO - J. Biol. Chem. VL - 279 IS - 35 N2 - N-cadherin is expressed throughout skeletal myogenesis and has been proposed to be involved in the differentiation program of myogenic precursors. Here, we further characterize the N-cadherin involvement and its mechanism of action at the onset of differentiation, through controlled N-cadherin activation by plating isolated C2 myoblasts on surfaces coated with a chimeric Ncad-Fc homophilic ligand (N-cadherin ectodomain fused to the immunoglobulin G Fc fragment). We show that N-cadherin activation substitutes for the cell density in myogenic differentiation by promoting myogenin and troponin T expression. In addition, N-cadherin adhesion participates to the associated cell cycle arrest through the nuclear accumulation of cyclin-dependent kinase inhibitors p21 and p27. Mouse primary myoblast cultures exhibited similar responses to N-cadherin as C2 cells. RNA interference knockdowns of the N-cadherin-associated cytoplasmic proteins p120 and beta-catenin produced opposite effects on the differentiation pathway. p120 silencing resulted in a decreased myogenic differentiation, associated with a reduction in cadherin-catenin content, which may explain its action on myogenic differentiation. beta-Catenin silencing led to a stimulatory effect on myogenin expression, without any effect on cell cycle. Our results demonstrate that N-cadherin adhesion may account for cell-cell contact-dependent cell cycle arrest and differentiation of myogenic cells, involving regulation through p120 and beta-catenins. SN - 0021-9258 UR - https://www.unboundmedicine.com/medline/citation/15194693/N-cadherin_activation_substitutes_for_the_cell_contact_control_in_cell_cycle_arrest_and_myogenic_differentiation:_involvement_of_p120_and_beta-catenin L2 - http://www.jbc.org/cgi/pmidlookup?view=long&pmid=15194693 DB - PRIME DP - Unbound Medicine ER -