4 results match your criteria: "Howard Hughes Medical Institute Stanford University School of Medicine[Affiliation]"
Curr Biol
October 2024
Howard Hughes Medical Institute Stanford University School of Medicine, Stanford, CA 02543, USA. Electronic address:
A critical question in biology is how new traits evolve, but studying this in wild animals remains challenging. Here, we probe the genetic basis of trait gain in sea robin fish, which have evolved specialized leg-like appendages for locomotion and digging along the ocean floor. We use genome sequencing, transcriptional profiling, and interspecific hybrid analysis to explore the molecular and developmental basis of leg formation.
View Article and Find Full Text PDFEMBO J
May 2016
Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute Stanford University School of Medicine, Stanford, CA, USA
Synaptic ribbons are large proteinaceous scaffolds at the active zone of ribbon synapses that are specialized for rapid sustained synaptic vesicles exocytosis. A single ribbon-specific protein is known, RIBEYE, suggesting that ribbons may be constructed from RIBEYE protein. RIBEYE knockdown in zebrafish, however, only reduced but did not eliminate ribbons, indicating a more ancillary role.
View Article and Find Full Text PDFEMBO Rep
October 2015
Department of Molecular and Cellular Physiology, Howard Hughes Medical Institute Stanford University School of Medicine, Stanford, CA, USA
Complexins are synaptic SNARE complex-binding proteins that cooperate with synaptotagmins in activating Ca(2+)-stimulated, synaptotagmin-dependent synaptic vesicle exocytosis and in clamping spontaneous, synaptotagmin-independent synaptic vesicle exocytosis. Here, we show that complexin sequences are conserved in some non-metazoan unicellular organisms and in all metazoans, suggesting that complexins are a universal feature of metazoans that predate metazoan evolution. We show that complexin from Nematostella vectensis, a cnidarian sea anemone far separated from mammals in metazoan evolution, functionally replaces mouse complexins in activating Ca(2+)-triggered exocytosis, but is unable to clamp spontaneous exocytosis.
View Article and Find Full Text PDFNeurobiol Dis
October 2000
Department of Neurobiology, Howard Hughes Medical Institute/Stanford University School of Medicine, Room 209, Sherman Fairchild Building, Stanford, California 94305, USA.