Elongation of C. elegans embryos requires stiffness and force to be specifically oriented in a coordinated manner in different cells.

Genetic analyses reveal that the loss of Lin28a causes axial shortening with mild skeletal transformations via decreased PRC1 at Hox genes, establishing a new pathway in the “Hox code.”.

Increasing levels of the growth factor Vegfa disrupt blood vessel branching morphogenesis and drive diameter increase by synchronizing Notch signalling fluctuations between endothelial cells.

Open-source software can untwist images of live Caenorhabditis elegans embryos, allowing epidermal and neuronal cell position and morphology to be examined in previously inaccessible developmental time periods.

The collinear activation of a subset of posterior Hox genes is responsible for establishing a Wnt/T activity gradient that is required to generate the complete body axis, and hence the full set of segments within a vertebrate embryo.

During axolotl spinal cord regeneration adult neural stem cells reactivate an embryonic neuroepithelial cell-like gene program that implements planar cell polarity to orient cell divisions, coupling polarized spinal cord growth with stem cell self-renewal.

During vertebrate axial extension, the tail bud originates from the activation of a developmental module in a subset of axial progenitors, concurrent but different to gastrulation.

Pluripotent stem cell differentiation provides insight into how neural crest subtypes of distinct axial identity are patterned in human embryos.

Genetic and molecular analyses show that FOXC1 and FOXC2 play a role in controlling lymphatic valve maintenance as key mediators of mechanotransduction to control cytoskeletal organization and RhoA/ROCK signaling.

EphA signaling plays dual opposite roles on axon dynamics in neurons, so it inhibits and promotes axon growth through ligand binding and receptor processing, respectively.