mTOR signaling regulates the morphology of a human-enriched neural stem cell population and thus contributes to the radial architecture of the developing human cortex with implications for neurodevelopmental disease.
Quantitative analyses associating the morphology of developing organs with dynamic gene expression patterns can reveal biological phenomena that cause malformations and malfunction but remain elusive to traditional qualitative assessments.
Analyses with genetically engineered mouse models in combination with biochemical approaches reveal a crucial role of the receptor tyrosine kinase Tie2 mediated signals in venogenesis via an Akt mediated regulation of COUP-TFII protein stabilization.
Improved 3D and 4D imaging of neurovascular processes across scales reveals new insights into eye disease mouse models and shows retinal vessels are significantly distorted using standard flat-mount confocal imaging.
Loss of function of the selective autophagy adaptor protein Alfy/Wdfy3 leads to profound wiring defects from the forebrain through to the spinal cord, highlighting the growing importance for macroautophagy in the developing brain.