Key result
Angptl1 expression localizes to connective tissue and cartilage, suggesting a developmental role despite no mutant phenotype.
Angptl1 expression is localized to connective tissue and cartilage during development, but its deficiency in mice does not produce an observable phenotype, possibly due to functional redundancy.
Angptl1 deficiency shows no phenotype in mice; leaves open its role in connective tissue development due to possible redundancy.
Angptl1, a member of the angiopoietin-related protein family, is known to regulate angiogenesis, but little is known of its potential role in other processes. To identify the expression pattern and possible role of angptl1 during embryogenesis, we used gene targeting to generate angptl1-deficient, nLacZ knockin mice. Staining for beta-galactosidase from embryonic day 9.5 to 6 months of age revealed that angptl1 was initially expressed in the paraxial mesoderm. Expression then shifted to intermuscular connective tissue (fascial plane), joint capsules, and perichondrium (laryngo-trachea, ribs, and long bones), but not the muscles. The vasculature, central and peripheral nervous systems, digestive, respiratory, and other major organ systems did not show any angptl1 expression. This expression pattern suggests that angptl1 is related to development of the connective tissue and cartilage. Lack of phenotype in mutant mice may be due to a functional redundancy from other related factors.
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Lai et al. (2007) studied Embryogenesis and connective tissue development. angptl1-deficient, nLacZ knockin was evaluated on angptl1 expression pattern. Angptl1 expression was localized to intermuscular connective tissue, joint capsules, and perichondrium, suggesting a role in connective tissue and cartilage development despite no mutant phenotype.
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