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

Abbas Jedariforoughi1, Rachel Burke1, Andrew Chesak1

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The temporal dynamics of c-Jun N-terminal kinase (JNK) activation influence downstream gene expression. Understanding JNK dynamics reveals how cells respond to stress and regulate cell death pathways.

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • c-Jun N-terminal kinase (JNK) is crucial for regulating cell death.
  • JNK activation dynamics influence cell survival versus cell death decisions under stress.
  • The link between JNK dynamics and downstream gene expression patterns is not fully understood.

Purpose of the Study:

  • To investigate how specific temporal dynamics of JNK activation impact downstream gene expression.
  • To explore the role of JNK dynamics in regulating transcription factors like c-Jun.
  • To elucidate the contribution of JNK dynamics to cellular responses to stress.

Main Methods:

  • Utilized anisomycin to induce sustained, transient, or pulsed JNK activation.
  • Assessed downstream gene expression patterns in response to varying JNK activation dynamics.
  • Employed ordinary differential equation (ODE) models to analyze gene expression patterns.
  • Examined mRNA stability and decay rates.

Main Results:

  • Distinct gene expression patterns emerged based on JNK activation dynamics.
  • ODE models indicated that mRNA stability mediates a subset of these gene expression clusters.
  • Experimental data on 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 profiles.
  • mRNA stability is a key mechanism by which JNK dynamics regulate gene expression.
  • JNK dynamics play a differential role in regulating cell death and inflammatory pathways.
  • These findings add to the understanding of JNK's role in cellular stress responses.