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JNK activation dynamics drive distinct gene expression patterns over time mediated by mRNA stability.

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    Cellular stress response is regulated by c-Jun N-terminal kinase (JNK) dynamics. Different JNK activation patterns influence downstream gene expression, impacting cell survival and inflammatory pathways.

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    Area of Science:

    • Cellular Biology
    • Molecular Biology
    • Systems Biology

    Background:

    • c-Jun N-terminal kinase (JNK) is crucial for regulating cell death.
    • JNK dynamics influence cell survival versus cell death decisions under stress.
    • The link between JNK dynamics and downstream gene expression via transcription factors like c-Jun requires further investigation.

    Purpose of the Study:

    • To investigate how specific JNK activation dynamics (sustained, transient, pulsed) affect downstream gene expression patterns.
    • To explore the role of mRNA stability in mediating gene expression responses to JNK dynamics.
    • To identify cellular pathways differentially regulated by JNK dynamics.

    Main Methods:

    • Utilized anisomycin, a JNK agonist, to induce distinct JNK activation dynamics in cells.
    • Assessed downstream gene expression patterns resulting from these dynamics.
    • Employed Ordinary Differential Equation (ODE) models and measured mRNA decay rates to analyze gene expression regulation.
    • Performed pathway enrichment analysis on identified gene clusters.

    Main Results:

    • Distinct gene expression patterns were observed, contingent upon the specific dynamics of JNK activation.
    • ODE models indicated that mRNA stability mediates a subset of these gene expression clusters.
    • Measured mRNA decay rates supported the role of mRNA stability.
    • Specific gene clusters were enriched in cell death and inflammatory signaling pathways.

    Conclusions:

    • JNK activation dynamics significantly shape downstream gene expression patterns.
    • mRNA stability is a key mechanism influencing gene expression responses to JNK signaling.
    • JNK dynamics contribute to the differential regulation of critical cellular pathways, including cell death and inflammation.
    • These findings add to the understanding of how JNK signaling controls cellular responses to stress.