His research explores how membrane lipids, membrane proteins, and the actin cytoskeleton cooperate to shape the plasma membrane and regulate cell behaviour. His laboratory is particularly known for its work on membrane blebs, uncovering how calcium signalling, membrane remodelling, and cytoskeletal dynamics coordinate the rapid structural changes that drive cellular processes such as migration and division.

Abstract 

Our laboratory is interested in how the major components of the cell surface — membrane lipids, membrane proteins, and the actin cytoskeleton — work together to generate specialized plasma membrane structures. Among these structures, we have recently focused on membrane blebs. 

The plasma membrane is normally supported by the cortical actin cytoskeleton. When this support is locally lost, intracellular pressure drives the membrane outward to form a spherical protrusion known as a bleb. Blebs are observed during apoptosis and cytokinesis, but are also actively used for cell migration by germ cells, cancer cells, and many amoeboid cells. Despite their apparently simple morphology, many aspects of bleb formation remain poorly understood. For example, how are the cytoplasm and plasma membrane locally reorganized to support rapid bleb expansion, and how is the actin cortex subsequently rebuilt? 

Using live-cell imaging of human epithelial cells, we have been investigating the molecular mechanisms underlying these dynamic processes. We first found that expanding blebs exhibit a local increase in cytoplasmic Ca²⁺ and increased cytoplasmic fluidity mediated by STIM–Orai1 signalling (Aoki et al., Nature Communications, 2021). More recently, we discovered that Ca²⁺ promotes the assembly of a CaMKII-centered protein supercomplex that generates osmotic force and contributes directly to bleb expansion (Fujii et al., The EMBO Journal, 2026). We have also identified transient membrane invaginations formed during bleb expansion that sequester curvature-preferring membrane proteins and thereby reorganize the plasma membrane during rapid deformation (Maekawa et al., PNAS, 2026). 

Together, these studies suggest that bleb formation is not simply a passive response to intracellular pressure, but a highly coordinated process coupling cytoplasmic organization, osmotic forces, membrane remodelling, and cytoskeletal dynamics.