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.
A theory predicts whether diffusion or direct transport establishes a more precise morphogen profile, and this prediction explains data from a wide variety of morphogens in two different organisms.
Experimental results in Drosophila support a model in which gene expression is fundamentally controlled by morphogens tuning the same transcription parameter for genes that are expressed in highly diverse patterns.
Live cell imaging demonstrates that the dynamics of ligand presentation influence signaling through two closely related morphogen signaling pathways in dramatically different ways.
Hedgehog acts as a morphogen by regulating proteolytic processing and activation of full-length Ci/Gli transcriptional effectors but can pattern Drosophila wing discs normally in the absence of regulated proteolytic processing.
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.
The requirement for WNT signaling in mesendoderm differentiation is temporally separate from that of ACTIVIN signaling and acts to switch the output of ACTIVIN/SMAD2 from pluripotency maintenance to mesendoderm patterning.
