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Molecular and Cellular Biology, August 2006, p. 6272-6282, Vol. 26, No. 16
0270-7306/06/$08.00+0     doi:10.1128/MCB.00472-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Cardiovascular and Craniofacial Defects in Crk-Null Mice

Tae-Ju Park,1 Kelli Boyd,2 and Tom Curran1*

Department of Developmental Neurobiology,1 Animal Resource Center, St. Jude Children's Research Hospital, Memphis, Tennessee 381052

Received 17 March 2006/ Returned for modification 15 April 2006/ Accepted 1 June 2006

The Crk adaptor protein, which is encoded by two splice variants termed CrkI and CrkII, contains both SH2 and SH3 domains but no catalytic region. It is thought to function in signal transduction processes involved in growth regulation, cell transformation, cell migration, and cell adhesion. Although the function of Crk has been studied in considerable detail in cell culture, its biological role in vivo is still unclear, and no Crk-knockout mouse model has been available. Therefore, we generated a complete null allele of Crk in mice by using the Cre-loxP recombination approach. The majority of Crk-null mice die at late stages of embryonic development, and the remainder succumb shortly after birth. Embryos lacking both CrkI and CrkII exhibited edema, hemorrhage, and cardiac defects. Immunohistochemical examination suggested that defects in vascular smooth muscle caused dilation and rupturing of blood vessels. Problems in nasal development and cleft palate were also observed. These data indicate that Crk is involved in cardiac and craniofacial development and that it plays an essential role in maintaining vascular integrity during embryonic development.

* Corresponding author. Mailing address: Children’s Hospital of Philadelphia, 517 Abramson Research Center, 3615 Civic Center Boulevard, Philadelphia, PA 19104-4318. Phone: (267) 462-2819. Fax: (215) 590-3709. E-mail: currant{at}email.chop.edu.

Molecular and Cellular Biology, August 2006, p. 6272-6282, Vol. 26, No. 16
0270-7306/06/$08.00+0     doi:10.1128/MCB.00472-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Seo, J.-H., Suenaga, A., Hatakeyama, M., Taiji, M., Imamoto, A. (2009). Structural and Functional Basis of a Role for CRKL in a Fibroblast Growth Factor 8-Induced Feed-Forward Loop. Mol. Cell. Biol. 29: 3076-3087 [Abstract] [Full Text]  
  • Meng, L., Bian, Z., Torensma, R., Von den Hoff, J.W. (2009). Biological Mechanisms in Palatogenesis and Cleft Palate. JDR 88: 22-33 [Abstract] [Full Text]  
  • Park, T.-J., Curran, T. (2008). Crk and Crk-Like Play Essential Overlapping Roles Downstream of Disabled-1 in the Reelin Pathway. J. Neurosci. 28: 13551-13562 [Abstract] [Full Text]  
  • Matsuki, T., Pramatarova, A., Howell, B. W. (2008). Reduction of Crk and CrkL expression blocks reelin-induced dendritogenesis. J. Cell Sci. 121: 1869-1875 [Abstract] [Full Text]  


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