Nf1 is required during early, but not late, cerebellar development to facilitate neuronal lamination, providing a potential therapeutic prevention strategy for NF1-associated developmental abnormalities.
Combined evidence of human genetics, in vitro cardiomyocyte differentiation, and mouse model indicates that SORBS2 is a regulator of second heart field development and its deficiency causes seemingly opposite atrial septal defects.
Diurnal variation loss of pineal allopregnanolone synthesis by light-at-night induces pituitary adenylate cyclase-activating polypeptide (PACAP) reduction and transcriptional PACAP repression in the cerebellum, with subsequent Purkinje cell death.
Experiments in zebrafish reveal a new role for a critical hypothalamic transcription factor, orthopedia, in controlling developmental neuropeptide balance in a discrete oxytocin-producing neuronal circuit whose disrupted development affects social behavior.
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.