Dynamic blockage in an exclusion process

Sahoo, Mamata; Dong, Jiajia; Klumpp, Stefan

doi:10.1088/1751-8113/48/1/015007

Cited by 16 publications

(26 citation statements)

References 42 publications

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“…Coupling this simple bulk rule to injection and extraction of motors at the boundaries gives rise to rich dynamical behavior, and the model has been extended to describe a wide range of physical and biological systems ( 27 – 33 ). Here, we extend the TASEP to include the interaction with roadblocks by building on earlier studies that considered a single roadblock ( 34 , 35 ), as well as multiple dynamic roadblocks in the so-called Bus-Route Model (BRM) ( 36 ).…”

Section: Methodsmentioning

confidence: 99%

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Berg

Depken

2017

Nucleic Acids Research

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During eukaryotic transcription, RNA polymerase (RNAP) translocates along DNA molecules covered with nucleosomes and other DNA binding proteins. Though the interactions between a single nucleosome and RNAP are by now fairly well understood, this understanding has not been synthesized into a description of transcription on crowded genes, where multiple RNAP transcribe through nucleosomes while preserving the nucleosome coverage. We here take a deductive modeling approach to establish the consequences of RNAP–nucleosome interactions for transcription in crowded environments. We show that under physiologically crowded conditions, the interactions of RNAP with nucleosomes induce a strong kinetic attraction between RNAP molecules, causing them to self-organize into stable and moving pelotons. The peloton formation quantitatively explains the observed nucleosome and RNAP depletion close to the initiation site on heavily transcribed genes. Pelotons further translate into short-timescale transcriptional bursts at termination, resulting in burst characteristics consistent with instances of bursty transcription observed in vivo. To facilitate experimental testing of our proposed mechanism, we present several analytic relations that make testable quantitative predictions.

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Section: Methodsmentioning

confidence: 99%

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Berg

Depken

2017

Nucleic Acids Research

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“…Coupling this simple bulk rule to injection and extraction of motors at the boundaries gives rise to rich dynamical behavior, and the model has been extended to describe a wide range of physical and biological systems (5,19,34,35,38,54,62). Here we extend the TASEP to include the interaction with roadblocks by building on earlier studies that considered a single roadblock (61,71), as well as multiple dynamic roadblocks in the so-called Bus-Route Model (BRM) (45).…”

Section: Methodsmentioning

confidence: 99%

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Berg

Depken

2016

Preprint

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During eukaryotic transcription, RNA polymerase (RNAP) translocates along DNA molecules covered with nucleosomes and other DNA binding proteins.Though the interactions between a single nucleosome and RNAP are by now fairly well understood, this understanding has not been synthesized into a description of transcription on crowded genes, where multiple RNAP transcribe through nucleosomes while preserving the nucleosome coverage. We here take a deductive modeling approach to establish the consequences of RNAP-nucleosome interactions for transcription in crowded environments.We show that under physiologically crowded conditions, the interactions of RNAP with nucleosomes induce a strong kinetic attraction between RNAP molecules, causing them to self-organize into stable and moving pelotons. The peloton formation quantitatively explains the observed nucleosome and RNAP depletion close to the initiation site on heavily transcribed genes. Pelotons further translate into short-timescale transcriptional bursts at termination, resulting in burst characteristics consistent with instances of bursty transcrip- 1. CC-BY-NC-ND 4.0 International license It is made available under a (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The copyright holder for this preprint . http://dx.doi.org/10.1101/065268 doi: bioRxiv preprint first posted online Aug. 18, 2016; tion observed in vivo. To facilitate experimental testing of our proposed mechanism, we present several analytic relations that make testable quantitative predictions.

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“…Our work closes a substantial gap in the field of driven diffusive systems. While the TASEP with quenched disorder [19,20,21,23,24], isolated dynamic defects [29,31,30,48], and disorder with particle-induced unbinding [32] has been studied before, we study for the first time the TASEP with random dynamic disorder. Although we do not progress beyond the mean field theory, we can reproduce many features (magnitude, skewness) of the CDR obtained from computer simulations.…”

Section: Discussionmentioning

confidence: 99%

“…A more complex model involving cooperation between polymerases in removing a roadblock has been applied to explain why transcription is not significantly compromised in the presence of DNA-bound proteins [27]. Non-biological applications include periodically switching traffic lights [28], obstacles that stochastically move and perform long range hops [29], or obstacles that bind and unbind stochastically to specific sites [30,31]. Inherent to these models is that similarly to the static defect case, the translational invariance is broken and thus congestion occurs at defect sites.…”

Section: Introductionmentioning

confidence: 99%

Totally asymmetric exclusion process with site-wise dynamic disorder

Waclaw¹,

Cholewa-Waclaw²,

Greulich³

2019

J. Phys. A: Math. Theor.

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We propose an extension of the totally asymmetric simple exclusion process (TASEP) in which particles hopping along a lattice can be blocked by obstacles that dynamically attach/detach from lattice sites. The model can be thought as TASEP with site-wise dynamic disorder. We consider two versions of defect dynamics: (i) defects can bind to any site, irrespective of particle occupation, (ii) defects only bind to sites which are not occupied by particles (particle-obstacle exclusion). In case (i) there is a symmetric, parabolic-like relationship between the current and particle density, as in the standard TASEP. Case (ii) leads to a skewed relationship for slow defect dynamics. We also show that the presence of defects induces particle clustering, despite the translation invariance of the system. For open boundaries the same three phases as for the standard TASEP are observed, albeit the position of phase boundaries is affected by the presence of obstacles. We develop a simple mean-field theory that captures the model's quantitative behaviour for periodic and open boundary conditions and yields good estimates for the current-density relationship, mean cluster sizes and phase boundaries. Lastly, we discuss an application of the model to the biological process of gene transcription.

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Dynamic blockage in an exclusion process

Cited by 16 publications

References 42 publications

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Crowding-induced transcriptional bursts dictate polymerase and nucleosome density profiles along genes

Totally asymmetric exclusion process with site-wise dynamic disorder

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