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Reproductive Sciences
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Article

Integrin Beta-4 Signaling Plays a Key Role in Mouse Embryogenesis

Jeffrey E. Roberts1, Sotiris N. Nikolopoulos2, Ozgur Oktem3, Filippo Giancotti2, and Kutluk Oktay3*

1 Pacific Centre for Reproductive Medicine
2 Memorial Sloan-Kettering Cancer Center
3 New York Medical College

* To whom correspondence should be addressed. E-mail: koktay{at}fertilitypreservation.org.


  Abstract

Integrins, by signaling between extracellular matrix and cell nucleus, serve critical roles in cell proliferation and survival. A knock-in mice was developed by a targeted deletion of the C-terminal segment of the cytoplasmic tail of {beta}4-integrin ({beta}4-1355T). The {beta}4-1355T mice had a longer gestational length, smaller litter sizes, lower fecundity rate, and higher frequency of early pregnancy loss. {beta}4-1355T embryos demonstrated a high degree of fragmentation and asymmetry, with fewer surviving to either a morula or blastocyst stage. In wild-type oocytes and embryos, {beta}1, {beta}4, and laminin-5 signals colocalized at the opposing surfaces of blastomeres and between the polar bodies and oocytes. Blastomeres within the {beta}4-1355T embryos were less cohesive, with a more diffuse expression of {beta}4 and laminin-5 compared with wild type. The {alpha}6{beta}4_laminin-5 interaction appears to be vital for maintaining the cohesiveness between the cells of the embryo. Deciphering the role of integrins such as {beta}4 in embryogenesis may help explain in vitro fertilization failures.

First published on December 15, 2008, doi:10.1177/1933719108325506

Reproductive Sciences 2009;16:286.

A more recent version of this article appeared on March 1, 2009

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