Colloquium

Asymmetric cell division, where daughter cells inherit unequal amounts of specific factors, is critical for development and cell fate specification. In polarized cells, where specific factors are segregated to opposite ends of the cell, asymmetric cell division occurs as a result of dynein-mediated centrosome positioning along the polarity axis. Early embryos of the nematode worm C. elegans polarize in response to fertilization and rely on proper centrosome positioning for cell fate specification and development. Depletion of certain proteins results in defective movement of centrosomes and the associated pronuclear complex. We developed a novel measure to characterize the oscillatory nature of these movement defects and demonstrated the presence of movement defects in response to cortically localized signaling proteins. We demonstrated that localization of the motor protein dynein, thought to be the primary driver of pronuclear movement, is not impaired in the presence of wobble in the early embryo. Ongoing research is combining experimental and theoretical approaches to identify possible mechanisms responsible for the impaired movement.

Place: Hybrid: Math, 501 and Zoom https://arizona.zoom.us/j/86997964863     Password:   Locute