Related Experiment Videos
Structure and DNA sequence of the mouse MnSOD gene
D DiSilvestre1, S R Kleeberger, J Johns
1Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287-7834, USA.
Summary
Manganese superoxide dismutase (Mn-SOD) protects mitochondria from oxidative damage. Genetic analysis in mice revealed no coding sequence differences, indicating variability in inflammatory responses is not due to altered Mn-SOD gene structure.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- Oxidative cellular damage contributes to chronic inflammation, aging, and cancer.
- Manganese superoxide dismutase (Mn-SOD) is crucial for mitochondrial protection against reactive oxygen species.
Purpose of the Study:
- To describe the genomic organization and DNA sequence of the murine MnSOD gene.
- To investigate if genetic variations in the MnSOD gene explain differences in pulmonary injury susceptibility to oxidants.
Main Methods:
- Sequencing of the murine MnSOD gene.
- Comparative analysis of MnSOD gene structure in oxidant-susceptible and resistant mouse strains (C57BL/6J and C3H/HeJ).
- Examination of both coding and noncoding sequences, including introns.
Main Results:
- The murine MnSOD gene contains four introns.
- No differences were found in the predicted amino acid sequence, transcript size, or steady-state level of Mn-SOD between susceptible and resistant mouse strains.
- A dC.dA polymorphism in intron 2 and a StyI RFLV in intron 4 were identified in the noncoding sequence.
Conclusions:
- Biologic variability in pulmonary inflammatory responses to ozone and hyperoxia is not caused by altered Mn-SOD gene structure.
- Sequence and mapping data of the MnSOD gene provide a foundation for further research into its role in disease variability.