Elsevier

Experimental Cell Research

Volume 230, Issue 1, 10 January 1997, Pages 28-37
Experimental Cell Research

Regular Article
BMP7 Null Mutation in Mice: Developmental Defects in Skeleton, Kidney, and Eye

https://doi.org/10.1006/excr.1996.3411Get rights and content

Abstract

While generatingbcl2α transgenic mice, we found some F2 offspring of one of the transgenic lines which were very small and had closed eyes at the time of weaning. These pups died within 1 month after birth. In order to determine the molecular basis of this phenotype, we screened a genomic library of the above transgenic line with a transgene-specific probe and found that theBmp7gene, a member of the TGFβ superfamily, was inactivated by insertional mutagenesis due to transgene integration. TheBmp7homozygous null condition in mice is a postnatal lethal mutation and is associated with various developmental defects: holes in the basisphenoid bone and the xyphoid cartilage, retarded ossification of bones, fused ribs and vertebrae, underdeveloped neural arches of the lumbar and sacral vertebrae, polydactyly of the hind limbs, a kinked tail, a reduced number of nephrons, polycystic kidney, lack of retinal pigmentation, and retarded lens development. These findings indicate that BMP7 is an important signaling molecule for normal development of the mammalian skeleton, kidney, and eye.

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