ADAMTS9 (a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 9) is a secreted metalloprotease involved in the cleavage of the extracellular matrix proteoglycan, versican, during development and aggrecan in cartilage. ADAMTS9 plays a role in normal gastrulation, craniofacial, cardiovascular and limb development, and melanoblast colonization of skin. Adamts9del knock-out mice have exons 5-8 deleted in the Adamts9 gene. Exons 5-8 encode a large portion of the catalytic domain including the protease active site. Deletion is believed to result in a frameshift and the absence of functional protein. Mice that are heterozygous for this allele are viable and fertile. Embryos homozygous for the mutation do not survive past gastrulation. E7.5 embryos appear compressed, lack mesoderm and have disorganized embryonic and extraembryonic tissue. Heterozygous mice develop cardiac valve anomalies and occasionally exhibit cloudy eyes in older mice.

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Adamts9del knock-out mice have exons 5-8 (including the protease active site) deleted in the a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 9 (Adamts9) gene. Embryos homozygous for the mutation do not survive past gastrulation. This strain may be useful for studying the regulation and consequences of extracellular matrix proteoglycans cleavage during development.

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