Cell biology of embryonic migration
- 10 June 2008
- journal article
- review article
- Published by Wiley in Birth Defects Research Part C: Embryo Today: Reviews
- Vol. 84 (2) , 102-122
- https://doi.org/10.1002/bdrc.20125
Abstract
Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni‐ and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton‐based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra‐ and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development. Birth Defects Research (Part C) 84:102–122, 2008.Keywords
This publication has 231 references indexed in Scilit:
- Attenuation of retinal vascular development and neovascularization in PECAM-1-deficient miceDevelopmental Biology, 2008
- Placental Defects in α7 Integrin Null MicePlacenta, 2007
- Activation of ROCK by RhoA is regulated by cell adhesion, shape, and cytoskeletal tensionExperimental Cell Research, 2007
- Filamin B deficiency in mice results in skeletal malformations and impaired microvascular developmentProceedings of the National Academy of Sciences, 2007
- Model systems for the study of heart development and diseaseSeminars in Cell & Developmental Biology, 2007
- The ARP2/3 complex: an actin nucleator comes of ageNature Reviews Molecular Cell Biology, 2006
- N-cadherin is required for neural crest remodeling of the cardiac outflow tractDevelopmental Biology, 2006
- Myosin II functions in actin-bundle turnover in neuronal growth conesNature Cell Biology, 2006
- Local force and geometry sensing regulate cell functionsNature Reviews Molecular Cell Biology, 2006
- Extensive Vasculogenesis, Angiogenesis, and Organogenesis Precede Lethality in Mice Lacking All αv IntegrinsCell, 1998