Lamellipodial

Lamellipodial refers to anything related to lamellipodia, which are broad, sheet-like protrusions at the leading edge of migrating animal cells. Lamellipodial activity is driven by rapid actin polymerization and is a central mechanism of cell locomotion.

The core structure is a branched actin network produced mainly by the Arp2/3 complex, activated by nucleation-promoting factors such as the WAVE/SCAR complex downstream of Rac family GTPases. New actin filaments grow from existing ones, creating a dense, dendritic mesh that pushes the membrane forward. Filament barbed ends near the membrane polymerize, while cross-linking proteins organize the network and regulatory proteins such as capping proteins and ADF/cofilin control filament length and turnover, enabling rapid remodeling.

Dynamics at the leading edge involve protrusion of the lamellipodium accompanied by retrograde actin flow. Adhesions form between the cell and substrate as the membrane advances, providing traction, while parts of the network are disassembled and recycled to allow continuing movement. The cycle of protrusion, adhesion, and retraction drives persistent migration.

Regulation and interactions: extracellular cues such as chemokines and growth factors activate signaling pathways that converge on Rac1 and the Arp2/3–WAVE/SCAR axis, coordinating lamellipodial formation with cytoskeletal rearrangements. Microtubules and adhesion complexes influence directionality and stability, and motor and contractile elements can modulate overall force generation.

Biological significance: lamellipodial protrusions are essential for directed cell migration in processes such as embryonic development, wound healing, and immune cell trafficking. They are also a focus of study in cancer metastasis and other pathologies involving altered cell motility.