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Pairs of spinal cord neurons arising from a shared progenitor get input from and make outputs to mostly different synaptic partners.

Activation of Notch receptors by ligands in the same cell (cis-activation) is a prevalent and functional mode of signaling in the Notch pathway, and co-exists with trans-activation and cis-inhibition.

Dephosphorylation of Notch1 intracellular domain by Eya1 leads to enhanced Notch signalling activity in the non-neuronal epibranchial placodal cells, revealing an essential regulation for the formation of proximal pharyngeal arches during mouse craniofacial development.

Interaction strength in Notch signaling determines lateral inhibition patterning and drives fate in the unidimensional cell arrangement of the zebrafish notochord.

Live imaging of the Notch co-activator Mastermind reveals that it promotes the formation of a dynamic transcription hub in Notch ON nuclei, conferring probabilistic transcription and providing a template for signal memory.

Notch1 activates autophagy to regulate the survival of T-regulatory cells from mice.

While Notch activation dedifferentiates newly differentiated muscle cells; it improves the function of muscle fiber as a niche-supporting cell of muscle stem cells.

Live-imaging of Notch-dependent transcription in vivo reveals that cell movements during gastrulation influence transcription levels, and do so downstream of Notch cleavage, illustrating the importance of crosstalk between mechanics and transcription in the context of embryonic development.

Fringe proteins modulate cis inhibitory, same-cell interactions between the Notch receptor and its ligands to control whether, and in which direction, cells can signal to one another.

Cell-cycle-dependent Notch signaling cooperates with temporal transcription factors to promote the progression of the temporal transcription factor cascade in Drosophila medulla neuroblasts.