Meeting Abstract
Dividing cells tend to round up through a loss of adhesion accompanied by increased intracellular tension. This process of mitotic rounding has a well characterized role in proper chromosome and spindle alignment. However, the potential impact of this process on cell signaling and fate specification has not been investigated. We study the impact of mitosis on cell signaling in the the invertebrate chordate, Ciona robusta. During Ciona development, four heart founder cells undergo an asymmetric division each giving rise to a tail muscle progenitor and a heart progenitor. Previous research has shown that the induction of the heart progenitor is caused by the polarized, mitotic redistribution of fibroblast growth factor receptors (FGFR) onto the adherent ventral membrane. In this study, we investigated the role of mitotic rounding in FGFR redistribution. To inhibit mitotic rounding, we employed 5-(N-Ethyl-N-isopropyl)amiloride (EIPA), a selective blocker of a Na+/H+ exchange pump. We found that application of EIPA just prior to founder cell division led to the expansion of the adherent membrane domain and depolarization of FGFR redistribution. Our results suggest that mitotic rounding can impact trafficking of membrane proteins including key signaling components, thereby influencing cell fate specification.
