Overview/Mission
DBCAB, formerly known as the Developmental Biology and Structural Variation Branch, focuses on deciphering the biological causes of structural congenital anomalies. Understanding the etiology of these errors in embryonic development provides the most promising route for improving prevention, diagnosis, and implementation of evidence-based treatments for patients and families affected by these rare diseases and conditions.
In addition to studies focused on identifying and elucidating the roles of gene variants, environmental perturbations, and other factors causing structural congenital anomalies, DBCAB supports studies to advance our understanding of the fundamental processes underlying formation and differentiation of the embryo. This basic knowledge is crucial for understanding how the process of embryogenesis can go awry.
Major program areas for the branch include early embryonic development and differentiation, biophysics/biomechanics of development, developmental neurobiology, organogenesis, regeneration, regenerative medicine, systems developmental biology, and developmental genetics, including genomic analysis of human structural congenital anomalies. The branch also administers the Gabriella Miller Kids First Pediatric Research Program, led by the NIH Common Fund, as well as NIH-wide coordination of research on congenital anomalies.
Highlights
- Science Update: Cellular metabolism regulates developmental rates, suggests NIIH-funded study
The study findings also suggest the potential to manipulate developmental rates at the cellular level. - Media Advisory: NIH-funded scientists generate a mouse embryo model that develops neural tubes
These embryoids offer a promising model system for research into factors affecting mammalian embryonic development and disease. - Some recent findings from DBCAB-supported researchers include the following:
- The Gene Ontology knowledgebase in 2023. This comprehensive resource concerning the functions of genes and gene products (proteins and noncoding RNAs) covers organisms and viruses and includes three components: a computational knowledge structure describing functional characteristics, annotations, and mechanistic models of molecular pathways. (PMID: 36866529)
- Reconstruction and deconstruction of human somitogenesis in vitro. This research demonstrates that major patterning modules involved in somitogenesis, including the clock and wavefront, anteroposterior polarity patterning and somite epithelialization, can be dissociated and operate independently within in vitro systems. (PMID: 36543321)
- Evolutionary divergent mTOR remodels translatome for tissue regeneration. Rapid activation of protein synthesis during injury response plays a crucial role in axolotl limb regeneration. The mTORC1 pathway is a key signal that mediates tissue regeneration and translational control in axolotls. An axolotl mTOR protein was engineered in human cells, inducing a state supporting rapid protein activation. This study provides another missing link in our understanding of vertebrate regenerative potential. (PMID: 37495694)