- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). [Guideline]
- AAutophagy 2016; 12(1):1-222
- N-cadherin activation substitutes for the cell contact control in cell cycle arrest and myogenic differentiation: involvement of p120 and beta-catenin. [Journal Article]
- JBJ Biol Chem 2004 Aug 27; 279(35):36795-802
- 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 involve…
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.
- Cadherin-based cell adhesion in neuromuscular development. [Review]
- BCBiol Cell 2002; 94(6):315-26
- The organisation and differentiation of striated skeletal muscles and their innervation is a particularly complex process implicating cells of mesodermic (myoblasts and fibroblasts) and neuroectoderr…
The organisation and differentiation of striated skeletal muscles and their innervation is a particularly complex process implicating cells of mesodermic (myoblasts and fibroblasts) and neuroectoderrmic origin (neurons and glial cells). Myogenic and motor neuron precursors, the two major cell types participating in the formation of the neuromuscular axis, migrate, segregate, reassociate and differentiate in a coordinated fashion. The subsequent organisation of muscle cells and the establishment of muscle innervation rely on a complex tissular and cellular architectural organisation, which cannot be understood without taking into account juxtacrine cell interactions, and especially cell adhesion. Cell adhesion receptors of the cadherin family are widely expressed and dynamically regulated in space and time throughout neuromuscular development. A single cell expresses in general more than one cadherin at its surface and it is the combination of these molecules and their level of expression that determine their action within a given cell population. We focused in this review on the expression and roles of classical cadherins in relation to muscle cell and motoneuron differentiation. We also review the latest results on the mode of action of cadherins allowing to propose cellular and molecular cues on the mechanisms by which these cell adhesion receptors control muscle and neuronal cell shape, migration and differentiation.
- [Not Available]. [Journal Article]
- CRC R Hebd Seances Acad Sci 1947 Jun 02; 224(22):1591