Evidence map›Paper›PMID 27630669›Full record

ArticleFrontiers in genetics2016

A Comparison of Deterministic and Stochastic Modeling Approaches for Biochemical Reaction Systems: On Fixed Points, Means, and Modes.

Sayuri K Hahl, Andreas Kremling

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Article in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

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0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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3 · Its place in the literature

Who cites it

24 citing papers in PubMed.

  1. Review
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  5. Theoretical and computational tools to model multistable gene regulatory networks.Reports on progress in physics. Physical Society (Great Britain) · 2023
    Review
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  19. Stochastic Simulation of Cellular Metabolism.IEEE access : practical innovations, open solutions · 2020
    Article
  20. Article
4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Sayuri K HahlSpecialty Division for Systems Biotechnology, Faculty of Mechanical Engineering, Technische Universität München Garching, Germany.
Andreas KremlingSpecialty Division for Systems Biotechnology, Faculty of Mechanical Engineering, Technische Universität München Garching, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the mathematical modeling of biochemical reactions, a convenient standard approach is to use ordinary differential equations (ODEs) that follow the law of mass action. However, this deterministic ansatz is based on simplifications; in particular, it neglects noise, which is inherent to biological processes. In contrast, the stochasticity of reactions is captured in detail by the discrete chemical master equation (CME). Therefore, the CME is frequently applied to mesoscopic systems, where copy numbers of involved components are small and random fluctuations are thus significant. Here, we compare those two common modeling approaches, aiming at identifying parallels and discrepancies between deterministic variables and possible stochastic counterparts like the mean or modes of the state space probability distribution. To that end, a mathematically flexible reaction scheme of autoregulatory gene expression is translated into the corresponding ODE and CME formulations. We show that in the thermodynamic limit, deterministic stable fixed points usually correspond well to the modes in the stationary probability distribution. However, this connection might be disrupted in small systems. The discrepancies are characterized and systematically traced back to the magnitude of the stoichiometric coefficients and to the presence of nonlinear reactions. These factors are found to synergistically promote large and highly asymmetric fluctuations. As a consequence, bistable but unimodal, and monostable but bimodal systems can emerge. This clearly challenges the role of ODE modeling in the description of cellular signaling and regulation, where some of the involved components usually occur in low copy numbers. Nevertheless, systems whose bimodality originates from deterministic bistability are found to sustain a more robust separation of the two states compared to bimodal, but monostable systems. In regulatory circuits that require precise coordination, ODE modeling is thus still expected to provide relevant indications on the underlying dynamics.

Indexed as

bimodalitybistabilitychemical master equationgene expressionordinary differential equationsprotein bursts

Identifiers

PMID27630669
PMCPMC5005346

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.