Kinetic Interference in Translational Control: A Path-Measure Framework for Collision-Triggered Transcript Decay
Abstract
I connect two literatures developed independently: the path-measure formulation of non-equilibrium statistical mechanics, where a trajectory action decomposes into a time-antisymmetric (entropic) and time-symmetric (frenetic) sector, and the stochastic modelling of ribosomal traffic on messenger RNA. The biological target is a proposed intervention -- antisense oligonucleotide (ASO) interference with wobble-uridine (U34) modification of transfer RNA -- whose intended effect is not to abolish translation but to perturb its timing, driving ribosome collisions and collision-triggered transcript decay preferentially on high-flux, codon-biased transcripts. Dynamical-activity and large-deviation analyses of generic lattice exclusion models -- notably the symmetric and totally asymmetric simple exclusion processes -- are well established. To my knowledge their formalization specifically for ribosomal traffic queues, translation elongation, and collision-triggered no-go decay remains unoccupied; this paper addresses that narrower gap, not the general one. Two claims here are load-bearing and untested. First, selectivity: transcripts whose loss is therapeutically desirable are separable, by vulnerable-codon-pair burden, from transcripts whose loss is toxic. Second, non-redundancy: the frenetic decomposition yields predictions, specific to ribosomal queueing and collision-triggered decay, not already obtainable from rate-level exclusion-process models or existing activity/large-deviation analyses of exclusion processes. This paper establishes neither. It specifies both as falsifiable tests with pre-registered decision rules, including outcomes under which the framework should be abandoned or narrowed. It is a research programme proposal, not a result. No new experimental, computational, or bioinformatic results are reported.
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BibTeX
@misc{segal2026kinetic,
title = {{Kinetic Interference in Translational Control: A Path-Measure Framework for Collision-Triggered Transcript Decay}},
author = {Shlomo Segal},
howpublished = {arXiv},
year = {2026},
month = sep,
doi = {10.48550/arxiv.2609.25536},
eprint = {2609.25536},
archivePrefix = {arXiv},
url = {https://arxiv.org/abs/2609.25536},
}
RIS
TY - UNPB
TI - Kinetic Interference in Translational Control: A Path-Measure Framework for Collision-Triggered Transcript Decay
AU - Shlomo Segal
PY - 2026
DA - 2026/09/22
PB - arXiv
DO - 10.48550/arxiv.2609.25536
UR - https://arxiv.org/abs/2609.25536
AB - I connect two literatures developed independently: the path-measure formulation of non-equilibrium statistical mechanics, where a trajectory action decomposes into a time-antisymmetric (entropic) and time-symmetric (frenetic) sector, and the stochastic modelling of ribosomal traffic on messenger RNA. The biological target is a proposed intervention -- antisense oligonucleotide (ASO) interference with wobble-uridine (U34) modification of transfer RNA -- whose intended effect is not to abolish translation but to perturb its timing, driving ribosome collisions and collision-triggered transcript decay preferentially on high-flux, codon-biased transcripts. Dynamical-activity and large-deviation analyses of generic lattice exclusion models -- notably the symmetric and totally asymmetric simple exclusion processes -- are well established. To my knowledge their formalization specifically for ribosomal traffic queues, translation elongation, and collision-triggered no-go decay remains unoccupied; this paper addresses that narrower gap, not the general one. Two claims here are load-bearing and untested. First, selectivity: transcripts whose loss is therapeutically desirable are separable, by vulnerable-codon-pair burden, from transcripts whose loss is toxic. Second, non-redundancy: the frenetic decomposition yields predictions, specific to ribosomal queueing and collision-triggered decay, not already obtainable from rate-level exclusion-process models or existing activity/large-deviation analyses of exclusion processes. This paper establishes neither. It specifies both as falsifiable tests with pre-registered decision rules, including outcomes under which the framework should be abandoned or narrowed. It is a research programme proposal, not a result. No new experimental, computational, or bioinformatic results are reported.
ER -