FGF morphogen gradient self-generates a recipient tissue-specific contour by feedback-regulating its cytoneme-mediated dispersion.

Diffusivity, extracellular interactions of Nodal ligands with the receptors and inhibitors, and selective ligand destruction collectively shape the Nodal morphogen gradient.

A kinetic model of morphogen interpretation is more suitable than classic threshold or ratchet models to understand how a signal gradient generates different target gene expression patterns.

Cell fates endowed by higher Bicoid concentration require input for longer duration, demonstrating a temporally non-linear morphogen-mediated pattern formation.

Live cell imaging demonstrates that the dynamics of ligand presentation influence signaling through two closely related morphogen signaling pathways in dramatically different ways.

Members of the BMP family of growth factors act as a reiterative code of distinct activities to direct the identities of different classes of sensory neurons in the spinal cord.

Interplay between protein concentration, DNA binding and remodeling of the chromatin landscape in early embryogenesis determines how a single transcription factor can specify multiple distinct gene expression states.

Proteolysis of lipidated N-terminal peptides that tether Hedgehog morphogens to the surface of source cells is absolutely required for their coupled release and bioactivation in vivo in Drosophila melanogaster.

Direct interaction between Hedgehog-sending and Hedgehog-receiving cytonemes is a fundamental mechanism for morphogen transfer and gradient establishment.

Glypican proteins, required for morphogen signalling in Drosophila wing development, are endocytosed and degraded by the feedback regulator Pentagone.