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.
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.
Maternal spindle transfer is a feasible approach to enhance embryonic developmental of compromised oocytes, which can represent a new strategy for patients with forms of infertility refractory to current treatments.
Neus Martínez-Abadías, Roger Mateu Estivill ... James Sharpe
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.
Dayana C Farhat, Matthew W Bowler ... Christopher Swale
The epitranscriptomic-driven mRNA polyadenylation pathway protects transcriptome integrity by restricting transcriptional read-throughs and RNA chimera formation in apicomplexan parasites and plants.
Daniel A Armendariz, Anjana Sundarrajan, Gary C Hon
Continuing advances in functional genomics will enable systematic characterization of how non-coding genetic variation at enhancers impacts developmental diseases.
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.
Scott A Rankin, Jeffrey D Steimle ... Aaron M Zorn
Epistatic analysis in Xenopus and mouse embryos reveals an evolutionarily conserved gene regulatory network downstream of the transcription factor Tbx5 and retinoic acid that coordinates cardiac and pulmonary development.
Georgia Panagiotakos, Christos Haveles ... Ricardo E Dolmetsch
The Timothy syndrome mutation in Cav1.2 gives rise to defects in neuronal differentiation by preventing a developmental switch in channel splicing and elevating calcium signaling in differentiating cells.