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Published on: February 18, 2011

Infectivity and methylation of retroviral genomes is correlated with expression in the animal

H Stuhlmann, D Jähner, R Jaenisch

    Cell
    |October 1, 1981
    PubMed

    Insights

    DNA methylation controls gene expression during animal development. Methylated endogenous Moloney leukemia virus (M-MuLV) genomes are inactive, while hypomethylated exogenous M-MuLV genomes are active, suggesting methylation

    Area of Science:

    • Molecular Biology
    • Developmental Biology
    • Epigenetics

    Background:

    • Gene expression regulation is crucial for animal development.
    • Retroviruses, like Moloney leukemia virus (M-MuLV), can integrate into the host genome.
    • Endogenous and exogenous viral genomes present distinct transmission and infection pathways.

    Purpose of the Study:

    • To investigate the role of DNA methylation in controlling gene expression during animal development.
    • To compare the methylation status and infectivity of endogenous versus exogenous M-MuLV genomes.
    • To elucidate the relationship between DNA methylation, viral genome activity, and gene expression.

    Main Methods:

    • Utilizing mouse substrains with germ line-transmitted M-MuLV.
    • Comparing endogenous (genetically transmitted) and exogenous (somatically acquired) M-MuLV genomes.
    • Assessing DNA methylation via Hha I restriction enzyme digestion and infectivity through DNA transfection assays.

    Main Results:

    • Endogenous M-MuLV genomes were highly methylated and non-infectious.
    • Exogenous M-MuLV copies were hypomethylated and infectious.
    • Viral genome activity, indicated by virus-specific RNA expression, correlated with hypomethylation and the presence of exogenous copies.

    Conclusions:

    • DNA methylation is strongly correlated with gene activity in animal development.
    • DNA methylation appears to play a causative role in regulating gene expression during development and differentiation.
    • The study provides evidence for epigenetic control of gene expression using viral models.

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