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C79 - Understanding craniofacial biology using a novel zebrafish mutant with elevated TGF-β signaling
Craniofacial anomalies account for nearly one-third of congenital birth defects worldwide, yet the developmental mechanisms underlying these disorders remain poorly understood.
C79 - Understanding craniofacial biology using a novel zebrafish mutant with elevated TGF-β signaling
Mentor: Jennifer Schumacher, Ph.D.
Craniofacial anomalies account for nearly one-third of congenital birth defects worldwide, yet the developmental mechanisms underlying these disorders remain poorly understood. Because much of the vertebrate craniofacial skeleton is derived from cranial neural crest cells (cNCCs), understanding how these cells migrate and organize is essential for identifying the causes of craniofacial malformations. During development, cNCC-derived chondrocytes normally align in a convergence-elongation pattern that is required for proper cartilage shape and growth. Previous work has shown that abnormal Transforming Growth Factor-beta (TGF-β) signaling can disrupt craniofacial development, but the mechanisms by which it affects cartilage organization are still unclear. This project uses zebrafish to investigate how hyperactive TGF-β signaling affects craniofacial cartilage patterning. Zebrafish are a powerful model for studying craniofacial development because their embryos are transparent, develop rapidly, and allow clear visualization of cartilage structures. In the Schumacher Lab, a novel chemically induced zebrafish mutant, pendulum (pen), was identified and found to exhibit hyperactive TGF-β signaling and abnormal craniofacial morphology. Preliminary Alcian blue staining showed that larval pen have shortened, widened, and disorganized craniofacial cartilage elements compared with sibling controls. We hypothesize that hyperactive TGF-β signaling in pen disrupts normal chondrocyte stacking, preventing cells from properly aligning into the convergence-elongation pattern. To test this, high-magnification images of cartilage from 96 hpf pen and sibling controls will be analyzed in ImageJ to quantify angular stacking arrangement. We expect pen to show reduced chondrocyte alignment and greater cartilage disorganization relative to controls. These findings will help clarify how TGF-β signaling contributes to cartilage organization during craniofacial development and may improve understanding of the developmental origins of craniofacial anomalies.