Date of Award

Spring 2021

Document Type

Restricted Thesis

Terms of Use

© 2021 Twan W. Sia. All rights reserved. Access to this work is restricted to users within the Swarthmore College network and may only be used for non-commercial, educational, and research purposes. Sharing with users outside of the Swarthmore College network is expressly prohibited. For all other uses, including reproduction and distribution, please contact the copyright holder.

Degree Name

Bachelor of Arts



First Advisor

Bradley Justin Davidson


Asymmetric division plays a key role in cell fate specification and tissue homeostasis. Recent studies have demonstrated that polarized trafficking of membrane proteins during cell division contributes to asymmetric division. Mitotic rounding is the biophysical process in which cells balloon up in mitotic entry to adopt a spherical shape. Mitotic rounding has been shown to influence cell division and development in a variety of ways, but rarely in the context of mitotic protein trafficking. During early Ciona robusta development, the pre-cardiac founder cells undergo asymmetric division to give rise to a ventral cardiac progenitor and a dorsal tail muscle progenitor. Previous work has shown that cardiac fate induction is a result of polarized redistribution of fibroblast growth factor receptors (FGFRs) to the ventral adherent membrane, and that FGFR trafficking occurs in a mitotic stage-dependent fashion. In our present work, we investigate the impact mitotic rounding has on FGFR redistribution. According to our model, mitotic rounding leads to shape changes that deadhere the pre-cardiac founder cells from the ventral epidermis. Localized focal adhesions polarizes FGFR redistribution to the ventral side, ultimately specifying cardiac cell fate in the ventral daughter post mitosis. To test this model, we blocked mitotic rounding using EIPA, an inhibitor of the Na+/H+ antiporter. This ion channel is responsible for generating the osmotic pressure that helps drive the ballooning of the cell. We found that EIPA treatment led to shorter, flatter cells during mitotic entry, showing that mitotic rounding was blocked. Through analyzing the distribution of FGFR, we found that loss of mitotic rounding led to the depolarization of FGFR in early mitosis. We also used induction assays to show that the loss of mitotic rounding resulted in a loss of asymmetric heart progenitor fate specification. Our results support a previously undocumented role for mitotic rounding in mitotic receptor trafficking and cell fate specification.