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Synchronization in stress p53 network.

Gurumayum Reenaroy Devi1, Md Jahoor Alam, R K Brojen Singh2

  • 1Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, New Delhi 110025, India.

Mathematical Medicine and Biology : a Journal of the IMA
|February 26, 2015
PubMed
Summary
This summary is machine-generated.

Nitric Oxide (NO) influences the p53-MDM2 network, causing distinct temporal behaviors like oscillation death or sustained oscillations. NO also mediates synchronization in coupled systems, with its dual role affecting stress and synchrony based on network coupling.

Keywords:
nitric oxidep53permutation entropystresssynchronization

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Area of Science:

  • Systems Biology
  • Biophysics
  • Computational Biology

Background:

  • The p53-MDM2 network is a crucial regulator of cellular stress response.
  • Nitric Oxide (NO) is a signaling molecule implicated in various cellular processes, including stress response and apoptosis.
  • Understanding the dynamics of this network under stress is vital for comprehending cellular fate decisions.

Purpose of the Study:

  • To investigate the temporal dynamics of p53 and MDM2 in a Nitric Oxide (NO)-induced stress network.
  • To analyze the synchronization phenomena in a 3D array of coupled p53-MDM2-NO systems.
  • To elucidate the specific roles of NO and noise in modulating network behavior and synchronization.

Main Methods:

  • Mathematical modeling of the p53-MDM2-NO regulatory network.
  • Analysis of single-system temporal behaviors (oscillation death, damped, and sustained oscillations) under varying NO-induced stress.
  • Simulation of coupled systems in a 3D array with nearest-neighbor diffusive coupling.
  • Investigation of correlation, permutation entropy, and synchronization (gamma) as functions of coupling strength (epsilon) and system size.
  • Deterministic and stochastic approaches were employed to analyze protein dynamics.

Main Results:

  • Three distinct temporal behaviors of p53 (oscillation death, damped, sustained oscillation) were identified, dependent on NO-induced stress levels.
  • System coupling (epsilon) increases correlation among systems, reaching a plateau.
  • Permutation entropy spectra for p53 and MDM2 differ due to NO's varied interactions.
  • NO plays a dual role: inducing stress at low/high coupling and promoting synchrony at moderate coupling.
  • Stochastic simulations reveal differences in synchronization (gamma) between p53 and MDM2, which diminish with increasing system size.

Conclusions:

  • The p53-MDM2-NO network exhibits complex dynamics, with NO significantly influencing both individual system behavior and inter-system synchronization.
  • NO's dual role in stress induction and synchrony mediation highlights its critical regulatory function in this network.
  • The findings provide insights into how cellular systems respond to stress and noise, with implications for understanding apoptosis.
  • Synchronization patterns are sensitive to coupling strength, system size, and the stochastic nature of the interactions.