04/20/2026
Only a few more Biology Seminars left for the semester! This Friday, Brennan Rosenthal will present on the role of Extracellular Matrix Proteins Fibronectin and Laminin in Axis Formation Within the Zebrafish Pineal Gland.
🔎Read the abstract below to learn more:
Incomplete closure of the anterior neural tube in mammals leads to anencephaly, a fatal neural tube defect (NTD). Our lab has found that zebrafish embryos deficient in two extracellular matrix (ECM) proteins, Laminin (Lam) and Fibronectin (Fn), display anencephaly-like phenotypes, though the mechanisms by which deficiencies in Lam and Fn trigger NTD are poorly understood. Previous work by Araya and colleagues suggests that these NTD could be caused by disorganized apicobasal polarity within neuroepithelium cells (Araya et al., Dev Dyn. 2016, 245:580-9). As cell polarity and axis formation are tightly linked, we hypothesize that axis formation within the anterior neural tube will also be disrupted in ECM-deficient mutants. This project assesses medial-lateral axis development within the neural tubes of Lam and Fn single and double mutants by observing expression of the protein Exorhodopsin (Exorh) within the pineal gland, a photosensitive protein which normally maps to the midline of the forebrain. Morphometric analysis showed that Exorh expression is significantly less linear in lamc1ti263a and lamb1apd110 mutants than in their WT siblings, and that lamc1ti263a, lamb1apd110, and fn1astop;fn1bstop genotypes display a reduction in the length: width ratio of the region of Exorh expression, indicating disruption of the normal medial-lateral axis. Additionally, lamc1ti263a, lamb1apd110, and fn1astop;fn1bstop genotypes display much higher instances of occlusion of the region of Exorh by melanocytes, suggesting that the pineal window is no longer excluding melanocytes from atop the pineal gland. These results imply that Lam and Fn facilitate coordination of adjacent tissue layers and orientation of cells to body axes during neurulation, providing context to further study of NTD in ECM-deficient mutants.