Compositional proofreading through critical self-tuning
Abstract
High-dimensional multicomponent systems, including immune and epigenetic repertoires, must selectively retain rare, beneficial components while purging a massive influx of suboptimal variants. We demonstrate that critical tuning of component control parameters through competition naturally implements proofreading in these systems. Competition for shared inputs pins the system to the marginal stability threshold of the most persistent species. This grants dominant species extended lifetimes, concentrating the population into dominant components while forcing less-stable variants into rapid drift-driven turnover. When aggregate drive exceeds a characteristic scale, this pinning fails, producing a non-selective state where component lifetimes scale as a universal power law with aggregate drive. Applying this framework to biological memory, we identify the hallmarks of this effect in plasma cell accumulation dynamics and propose that de-pinning transitions may represent failure points across biological domains, including cancer, immunodeficiencies, and the aberrant activation of harmful genomic elements during ageing.
Versions
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BibTeX
@misc{karin2026compositional,
title = {{Compositional proofreading through critical self-tuning}},
author = {Omer Karin},
howpublished = {arXiv},
year = {2026},
month = jun,
doi = {10.48550/arxiv.2606.10636},
eprint = {2606.10636},
archivePrefix = {arXiv},
url = {https://arxiv.org/abs/2606.10636},
note = {CC BY 4.0},
}
RIS
TY - UNPB
TI - Compositional proofreading through critical self-tuning
AU - Omer Karin
PY - 2026
DA - 2026/06/09
PB - arXiv
DO - 10.48550/arxiv.2606.10636
UR - https://arxiv.org/abs/2606.10636
AB - High-dimensional multicomponent systems, including immune and epigenetic repertoires, must selectively retain rare, beneficial components while purging a massive influx of suboptimal variants. We demonstrate that critical tuning of component control parameters through competition naturally implements proofreading in these systems. Competition for shared inputs pins the system to the marginal stability threshold of the most persistent species. This grants dominant species extended lifetimes, concentrating the population into dominant components while forcing less-stable variants into rapid drift-driven turnover. When aggregate drive exceeds a characteristic scale, this pinning fails, producing a non-selective state where component lifetimes scale as a universal power law with aggregate drive. Applying this framework to biological memory, we identify the hallmarks of this effect in plasma cell accumulation dynamics and propose that de-pinning transitions may represent failure points across biological domains, including cancer, immunodeficiencies, and the aberrant activation of harmful genomic elements during ageing.
ER -