Presentation description

Zebrafish embryos are an ideal model for in vivo studies of early developmental events due to their genetic tractability and transparency. Common wildtype strains however become pigmented, limiting visualization of developmental events past embryogenesis. roy orbison (roy) mutants lack iridophores, a reflective pigment cell, and have less melanin filled melanophores, rendering them partially transparent through adulthood, allowing for observation of tissues, such as vascular structures. roy and other pigment mutants have been extensively used in non-pigment related studies. However, roy carries a mutation in mpv17, which encodes a protein involved in mitochondrial homeostasis expressed in several non-pigment cells. While previous research comparing roy to wildtype strains showed roy mitochondria behave differently in the lateral line system, whether this mutation affects vascular development is unknown. We characterized and compared cephalic vascular phenotypes in roy and wildtype, focusing on blood flow defects and the presence or persistence of brain hemorrhage. My analysis has shown no observable differences in brain hemorrhage rates between roy and wildtype strains, but we are continuing further analysis using transgenic zebrafish lines labeling vasculature to identify subtler phenotypes such as vessel integrity, specifically in the meninges. Finally, we are using MitoTracker to quantitatively measure meningeal mitochondrial mass and activity at the cellular level to further explore the implifications of the mpv17 mutation on meningeal vasculature. This work will establish whether genetic background impacts meningeal vasculature as shown in other systems.