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First published online 26 January 2005
doi: 10.1242/dev.01673

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Distinct developmental programs require different levels of Bmp signaling during mouse retinal development

Deepa Murali^1,2,*, Shunichi Yoshikawa^1,*, Rebecca R. Corrigan^1,2, Daniel J. Plas³, Michael C. Crair³, Guillermo Oliver⁴, Karen M. Lyons⁵, Yuji Mishina⁶ and Yasuhide Furuta^1,2,

¹ Department of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA
² Program in Genes and Development, Graduate School of Biomedical Sciences (GSBS), University of Texas-Houston, Health Sciences Center and M.D. Anderson Cancer Center, Houston, TX 77030, USA
³ Department of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA
⁴ Department of Genetics, St Jude Children's Research Hospital, Memphis, TN 38105, USA
⁵ Departments of Molecular, Cell and Developmental Biology, Orthopedic Surgery, and Biological Chemistry, University of California, Los Angeles, CA 90095, USA
⁶ Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health and Safety/NIH, Research Triangle Park, NC 27709, USA

Author for correspondence (e-mail: yfuruta{at}mdanderson.org)

Accepted 22 December 2004

The Bmp family of secreted signaling molecules is implicated in multiple aspects of embryonic development. However, the cell-type-specific requirements for this signaling pathway are often obscure in the context of complex embryonic tissue interactions. To define the cell-autonomous requirements for Bmp signaling, we have used a Cre-loxP strategy to delete Bmp receptor function specifically within the developing mouse retina. Disruption of a Bmp type I receptor gene, Bmpr1a, leads to no detectable eye abnormality. Further reduction of Bmp receptor activity by removing one functional copy of another Bmp type I receptor gene, Bmpr1b, in the retina-specific Bmpr1a mutant background, results in abnormal retinal dorsoventral patterning. Double mutants completely lacking both of these genes exhibit severe eye defects characterized by reduced growth of embryonic retina and failure of retinal neurogenesis. These studies provide direct genetic evidence that Bmpr1a and Bmpr1b play redundant roles during retinal development, and that different threshold levels of Bmp signaling regulate distinct developmental programs such as patterning, growth and differentiation of the retina.

Key words: Bmpr1a, Bmpr1b, Bmp signaling, Mutant mouse, Retinal patterning, Retinal growth, Retinal neurogenesis

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