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. 1999 Nov 29;147(5):1109–1122. doi: 10.1083/jcb.147.5.1109

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© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Skeletal abnormalities in perlecan-null embryos. (A) Lateral view of E16.5 normal, heterozygous, and perlecan-null (−/−^a and −/−^b) embryos. Loss of perlecan results in disproportionate dwarfism with short limbs, neck, and snout. Some homozygotes have domed skull (−/−^a), others lack the roof of skull and exhibit exencephaly (−/−^b). (B) Alcian blue/alizarin red stained skeletons of normal, heterozygous, and perlecan-null (−/−^a and −/−^b) E17.5 embryos. The skeleton of heterozygotes is normal. The spine of homozygous mutants is short and displays severe kyphoscoliosis, the thorax is narrow, and the ribs, vertebrae, and long bones are malformed. Embryos with exencephaly (−/−^b) lack frontal and parietal bones of the skull. (C–F) Comparative histological analysis of developing hindlimbs from normal (C and E) and homozygotes (D and F). Sagittal sections from E14 (C and D) and E16.5 (E and F) embryos stained with hematoxylin/eosin. At E14, the mutant tibia (ti) and fibula (fi) are short, thick, and curved (D). At E16.5, the mutant tibia (F) is short and thick, the metaphyseal bone is extremely reduced, and the growth plate is disorganized. Abbreviations: ec, epiphyseal cartilage; p, zone of proliferative chondrocytes; h, zone of hypertrophic chondrocytes; and bc, bone cavity. Bar: (C–F) 100 μm.