Developmental regulation of beta-galactoside specific lectin in postnatal rat lung
Date of Award
Doctor of Philosophy (Ph.D.)
First Committee Member
Philip L. Whitney, Committee Chair
Rat lung lectin is an endogenous dimeric $\beta$-galactoside-binding protein of subunit molecular weight 14,000 that exhibits a developmentally-regulated peak of hemagglutinating activity at postnatal days 10 to 12. This thesis examines mechanisms that might be responsible for the changes in the activity of rat lung lectin during the second postnatal week and asks if its activity or turnover can be modulated by treatment of rat pups with a glucocorticosteroid hormone (dexamethasone). These studies indicated the peak of lectin activity (U/mg protein) that occurred at age 12 days was brought about by two means: a three-fold increase in the activity of the lectin molecule itself (U/$\mu$g lectin) that occurred at age 8 days and a 1.5-fold increase in the absolute rate of lectin synthesis at age 11 days. The decline in lectin activity was effected by a decrease in its rate of synthesis, return to the baseline level of activation, and an increased rate of degradation. Treatment of rat pups with dexamethasone diminished the peak of lectin activity (U/mg protein) by about 25%. This effect of dexamethasone was due to a complete prevention of the increase in activity of the lectin molecule (U/$\mu$g lectin) and a premature increase in the rate of lectin degradation. To determine if the changes in lectin synthesis were regulated at the level of transcription, translation, or both, a rat lung cDNA library was generated and a full-length lectin cDNA was cloned. A probe made from a fragment of the cDNA was used to measure lung lectin mRNA concentration. Lung lectin mRNA/mg DNA increased to a peak at age 6 days; dexamethasone treatment aborted the increase in lectin mRNA concentration, quickly returning it to baseline levels. Translational efficiency (lectin synthesis/lectin mRNA) was maximal at day 11 in lungs from control rats and was significantly increased in lungs from dexamethasone-treated rats at days 11 and 15. These findings indicate that postnatal rat lung lectin gene expression is regulated at both pretranslational and translational levels and that dexamethasone treatment can modulate regulation at both levels.
Clerch, Linda Biadasz, "Developmental regulation of beta-galactoside specific lectin in postnatal rat lung" (1988). Dissertations from ProQuest. 2676.