期刊
GENES & DEVELOPMENT
卷 21, 期 17, 页码 2131-2136出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1561507
关键词
neural crest; migration; adhesion; Rap; development; zebrafish
资金
- NATIONAL CANCER INSTITUTE [R01CA104605, F32CA117737] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL079267] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R00NS058608, K99NS058608] Funding Source: NIH RePORTER
- NCI NIH HHS [F32 CA117737, CA104605, R01 CA104605, CA117737] Funding Source: Medline
- NHLBI NIH HHS [R01 HL079267, HL079267] Funding Source: Medline
- NINDS NIH HHS [K99 NS058608-01, K99 NS058608, K99NS058608, R00 NS058608, R00 NS058608-03, K99 NS058608-02] Funding Source: Medline
- PHS HHS [P01 95281] Funding Source: Medline
The neural crest (NC) is a highly motile cell population that gives rise to multiple tissue lineages during vertebrate embryogenesis. Here, we identify a novel effector of the small GTPase Rap, called RADIL, and show that it is required for cell adhesion and migration. Knockdown of radii in the zebrafish model results in multiple defects in NC-derived lineages such as cartilage, pigment cells, and enteric neurons. We specifically show that these defects are primarily due to the diminished migratory capacity of NC cells. The identification of RADIL as a regulator of NC migration defines a role for the Rap pathway in this process.
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