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Molecular and Cellular Biology, August 2004, p. 7113-7129, Vol. 24, No. 16
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.16.7113-7129.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Defective Extraembryonic Angiogenesis in Mice Lacking LBP-1a, a Member of the grainyhead Family of Transcription Factors

Vishwas Parekh,1 Amy McEwen,1 Virginia Barbour,1 Yutaka Takahashi,2 Jerold E. Rehg,3 Stephen M. Jane,4 and John M. Cunningham1,5*

Departments of Hematology/Oncology,1 Biochemistry,2 Pathology, St. Jude Children's Research Hospital,3 Departments of Molecular Sciences and Pediatrics, University of Tennessee, Memphis, Tennessee 38105,5 Rotary Bone Marrow Research Laboratory, Royal Melbourne Hospital Research Foundation, Parkville, Victoria 3050, Australia4

Received 20 October 2003/ Returned for modification 3 January 2004/ Accepted 3 May 2004

LBP-1a and CP2 are ubiquitously expressed members of the grainyhead transcription factor family, sharing significant sequence homology, a common DNA binding motif, and modulating a range of key regulatory and structural genes. We have reported previously that CP2-null mice are viable with no obvious abnormality. LBP-1a provides redundant function in this context. We show here that mice lacking LBP-1a expression develop intrauterine growth retardation at embryonic day 10.5, culminating in death 1 day later. No focal intraembryonic cause for this CP2-independent defect is evident. In contrast, a significant reduction in the thickness of the labyrinthine layer of the placenta is observed in LBP-1a–/– animals. However, expression of trophoblast differentiation markers is unperturbed in this context, and complementation studies utilizing tetraploid wild-type cells failed to rescue or ameliorate the LBP-1a–/– phenotype, excluding a primary trophoblast defect. An explanation for these observations is provided by the prominent angiogenic defect observed in the mutant placentas. LBP-1a–/– allantoic blood vessels fail to penetrate deeply and branch into the complex embryonic vasculature characteristic of the normal placenta. Interestingly, a similar defect in angiogenesis is observed in the yolk sac vasculature, primary endothelial cell-lined capillary tubes, although present, failed to connect into a characteristic intricate vascular network. Collectively, these results demonstrate that LBP-1a plays a critical role in the regulation of extraembryonic angiogenesis.

* Corresponding author. Mailing address: Department of Hematology/Oncology, St. Jude Children's Research Hospital, 332 N. Lauderdale, Memphis, TN 38105. Phone: (901) 495-2746. Fax: (901) 495-2176. E-mail: john.cunningham{at}stjude.org.

Molecular and Cellular Biology, August 2004, p. 7113-7129, Vol. 24, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.16.7113-7129.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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