Journal
NATURE REVIEWS MOLECULAR CELL BIOLOGY
Volume 15, Issue 9, Pages 577-590Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrm3861
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Funding
- BBSRC [BB/G00319X/1, BB/F011431/1, BB/J000590/1]
- Wellcome Trust [077429/Z/05/Z, 082907/Z/07/Z]
- Agence Nationale de la Recherche
- Institut National du Cancer
- Association pour la Recherche sur le Cancer
- Biotechnology and Biological Sciences Research Council [BB/G00319X/1, BB/F011431/1, BB/J000590/1] Funding Source: researchfish
- Medical Research Council [1522273] Funding Source: researchfish
- BBSRC [BB/J000590/1, BB/F011431/1, BB/G00319X/1] Funding Source: UKRI
- Wellcome Trust [082907/Z/07/Z] Funding Source: Wellcome Trust
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Membrane protrusions at the leading edge of cells, known as lamellipodia, drive cell migration in many normal and pathological situations. Lamellipodial protrusion is powered by actin polymerization, which is mediated by the actin-related protein 2/3 (ARP2/3)-induced nucleation of branched actin networks and the elongation of actin filaments. Recently, advances have been made in our understanding of positive and negative ARP2/3 regulators (such as the SCAR/WAVE (SCAR/WASP family verprolin-homologous protein) complex and Arpin, respectively) and of proteins that control actin branch stability (such as glial maturation factor (GMF)) or actin filament elongation (such as ENA/VASP proteins) in lamellipodium dynamics and cell migration. This Review highlights how the balance between actin filament branching and elongation, and between the positive and negative feedback loops that regulate these activities, determines lamellipodial persistence. Importantly, directional persistence, which results from lamellipodial persistence, emerges as a critical factor in steering cell migration.
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