Soluble β-Galactoside Specific Lectin is Developmentally Regulated in Lungs of Neonatal Black Mice and Beige Mice

Abstract

The beige mouse, a mutant of the C57 black mouse, is best known as a model of the Chediak-Higashi syndrome. Recently, it was found that alveolar maturation in neonatal beige mice is impaired, resulting in abnormally large alveoli. In guinea pigs, hamsters, and rats there is an elevated activity of a soluble, 0-galactoside-binding lectin in lungs at the age when alveolar maturation is in progress. Our present studies were done to find out if the temporal relationship between elevated lectin activity and alveolar maturation also occurs in mice and, further, if the impaired alveolar maturation in beige mice might be linked to the lectin. We found that the temporal relationship between lectin activity and alveolar maturation is also present in black and beige mice, with a peak in specific lectin activity occurring at about 8 days after birth. We also found that the major lectin purified from black or beige mice has essentially the same subunit molecular weight, isoelectric point, and amino acid composition. In conclusion, we found nothing abnormal about the lectin or its developmental regulation that can explain the impaired alveolar maturation in neonatal beige mice. The results do not rule out the possibility of an important role for the lectin in normal lung development or the possibility that some aspect of function or localization of the lectin or its ligands, not related to total lung lectin hemagglutinating activity, may be altered in the beige mouse.