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Rat lung lectin gene expression is regulated developmentally and by dexamethasone
L B Clerch1, P Whitney, D Massaro
1Pulmonary Research Laboratories, Calvin and Flavia Oak Asthma Research and Treatment Facility, University of Miami School of Medicine 33136.
The American Journal of Physiology
|March 1, 1989
Summary
Rat lung lectin mRNA levels peak early postnatally, but dexamethasone treatment prevents this rise. This suggests pretranslational regulation of lectin synthesis, with glucocorticoids impacting mRNA concentration and translational efficiency.
Area of Science:
- Biochemistry
- Developmental Biology
- Molecular Biology
Background:
- Soluble beta-galactoside-binding proteins (lectins) exhibit developmentally regulated cell-agglutinating activity in mammalian organs.
- The specific gene expression alterations driving this developmental regulation remain largely uncharacterized.
- Rat lung possesses a dimeric beta-galactoside-binding protein with a postnatal hemagglutination activity peak, partly due to increased lectin synthesis.
Purpose of the Study:
- To investigate the molecular mechanisms underlying the developmental regulation of beta-galactoside-binding protein (lectin) synthesis in rat lung.
- To determine the role of gene expression and translational control in the postnatal increase of lectin activity.
- To examine the effects of dexamethasone on lectin gene expression and synthesis.
Main Methods:
- Northern blot analysis to quantify rat lung lectin mRNA concentration over postnatal development.
- Southern blot analysis to assess the potential presence of multiple lectin genes.
- Analysis of lectin subunit size and mRNA hybridization patterns to confirm the measurement of a single gene product.
Main Results:
- Rat lung lectin mRNA concentration peaked at 6 days postnatally.
- Dexamethasone treatment inhibited the postnatal increase in lectin mRNA concentration.
- Evidence indicated the measurement of a single lectin gene product, despite Southern blot compatibility with multiple genes.
- Postnatal lectin synthesis increase is mediated by pretranslational events and enhanced translational efficiency.
- Dexamethasone impaired lectin mRNA increase but enhanced translational efficiency.
Conclusions:
- The postnatal surge in rat lung lectin synthesis is primarily regulated at the pretranslational level, involving both mRNA accumulation and translational efficiency.
- Dexamethasone exerts differential effects, suppressing mRNA levels while promoting translational efficiency, thereby modulating overall lectin production.