Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.
Molecular labeling, electrophysiology and calcium imaging have revealed a novel switching of neurotransmitter at the frog neuromuscular junction where motoneurons transiently release glutamate before acetylcholine at synapses on developing hindlimb muscles at the onset of metamorphosis.
Soon after fertilisation, a critical portion of the embryonic genome is switched on through the actions of maternally inherited Stella, in part through controlling the activation of transposable elements.
Transcription factors that specify the identity of individual neuron types via activating terminal differentiation gene batteries also restrict cellular plasticity via altering the chromatin landscape.
C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.