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Competing constraints shape the nonequilibrium limits of cellular decision-making. | LitMetric

Competing constraints shape the nonequilibrium limits of cellular decision-making.

Proc Natl Acad Sci U S A

Biophysics Graduate Group, University of California, Berkeley, CA 904720.

Published: March 2023

AI Article Synopsis

  • Gene regulation is essential for cellular function, but current models struggle to predict transcriptional control from molecular interactions, especially in eukaryotes where ATP-dependent processes are involved.
  • Traditional thermodynamic models work for bacteria but fail to account for how eukaryotic gene circuits respond to different levels of transcription factors.
  • Investigating kinetic models shows that using energy dissipation can enhance how quickly genes transmit information; however, the effectiveness depends on whether interference from noncognate activators is low or high, leading to different regulatory strategies.

Article Abstract

Gene regulation is central to cellular function. Yet, despite decades of work, we lack quantitative models that can predict how transcriptional control emerges from molecular interactions at the gene locus. Thermodynamic models of transcription, which assume that gene circuits operate at equilibrium, have previously been employed with considerable success in the context of bacterial systems. However, the presence of ATP-dependent processes within the eukaryotic transcriptional cycle suggests that equilibrium models may be insufficient to capture how eukaryotic gene circuits sense and respond to input transcription factor concentrations. Here, we employ simple kinetic models of transcription to investigate how energy dissipation within the transcriptional cycle impacts the rate at which genes transmit information and drive cellular decisions. We find that biologically plausible levels of energy input can lead to significant gains in how rapidly gene loci transmit information but discover that the regulatory mechanisms underlying these gains change depending on the level of interference from noncognate activator binding. When interference is low, information is maximized by harnessing energy to push the sensitivity of the transcriptional response to input transcription factors beyond its equilibrium limits. Conversely, when interference is high, conditions favor genes that harness energy to increase transcriptional specificity by proofreading activator identity. Our analysis further reveals that equilibrium gene regulatory mechanisms break down as transcriptional interference increases, suggesting that energy dissipation may be indispensable in systems where noncognate factor interference is sufficiently large.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10013869PMC
http://dx.doi.org/10.1073/pnas.2211203120DOI Listing

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