Journal
DEVELOPMENTAL CELL
Volume 21, Issue 4, Pages 722-734Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2011.07.008
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Funding
- Medical Research Council UK [G117/569]
- Cancer Research UK
- Association for International Cancer Research [11-0119, 09-0227]
- NIH [HL059561]
- Ligue national contre le cancer (Equipe labellisee)
- [CA142928]
- Cancer Research UK [12481] Funding Source: researchfish
- Medical Research Council [MC_U127527200, MC_PC_U127527200, G117/569, G0901991] Funding Source: researchfish
- Worldwide Cancer Research [11-0119] Funding Source: researchfish
- MRC [G117/569, MC_PC_U127527200, MC_U127527200, G0901991] Funding Source: UKRI
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During embryogenesis, melanoblasts proliferate and migrate ventrally through the developing dermis and epidermis as single cells. Targeted deletion of Rac1 in melanoblasts during embryogenesis causes defects in migration, cell-cycle progression, and cytokinesis. Rac1 null cells migrate markedly less efficiently, but surprisingly, global steering, crossing the dermal/epidermal junction, and homing to hair follicles occur normally. Melanoblasts navigate in the epidermis using two classes of protrusion: short stubs and long pseudopods. Short stubs are distinct from blebs and are driven by actin assembly but are independent of Rac1, Arp2/3 complex, myosin, or microtubules. Rac1 positively regulates the frequency of initiation of long pseudopods, which promote migration speed and directional plasticity. Scar/WAVE and Arp2/3 complex drive actin assembly for long pseudopod extension, which also depends on microtubule dynamics. Myosin contractility balances the extension of long pseudopods by effecting retraction and allowing force generation for movement through the complex 3D epidermal environment.
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