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Molecular and Cellular Biology, November 2005, p. 9318-9323, Vol. 25, No. 21
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.21.9318-9323.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Clathrin Adaptor AP-2 Is Essential for Early Embryonal Development

Takashi Mitsunari,1,2 Fubito Nakatsu,1,2 Noriko Shioda,2 Paul E. Love,3 Alexander Grinberg,3 Juan S. Bonifacino,4 and Hiroshi Ohno1,2,5*

Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, 1-7-22 Suehiro, Tsurumi, Yokohama, Kanagawa 230-0045, Japan,1 Cancer Research Institute, Kanazawa University, 13-1 Takaramachi, Kanazawa, Ishikawa 920-0934, Japan,2 Laboratory of Mammalian Genes and Development,3 Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892,4 Supramolecular Biology, International Graduate School of Arts and Sciences, Yokohama City University, 1-7-22 Suehiro, Tsurumi, Yokohama, Kanagawa 230-0045, Japan5

Received 5 July 2005/ Returned for modification 3 August 2005/ Accepted 13 August 2005

The heterotetrameric adaptor protein (AP) complexes AP-1, AP-2, AP-3, and AP-4 play key roles in transport vesicle formation and cargo sorting in post-Golgi trafficking pathways. Studies on cultured mammalian cells have shown that AP-2 mediates rapid endocytosis of a subset of plasma membrane receptors. To determine whether this function is essential in the context of a whole mammalian organism, we carried out targeted disruption of the gene encoding the µ2 subunit of AP-2 in the mouse. We found that µ2 heterozygous mutant mice were viable and had an apparently normal phenotype. In contrast, no µ2 homozygous mutant embryos were identified among blastocysts from intercrossed heterozygotes, indicating that µ2-deficient embryos die before day 3.5 postcoitus (E3.5). These results indicate that AP-2 is indispensable for early embryonic development, which might be due to its requirement for cell viability.

* Corresponding author. Mailing address: Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, 1-7-22 Suehiro, Tsurumi, Yokohama, Kanagawa 230-0045, Japan. Phone: 81 45 503 7031. Fax: 81 45 503 7030. E-mail: ohno{at}rcai.riken.jp.

Molecular and Cellular Biology, November 2005, p. 9318-9323, Vol. 25, No. 21
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.21.9318-9323.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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