ArticlePLoS computational biology2020
Strong intracellular signal inactivation produces sharper and more robust signaling from cell membrane to nucleus.
Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 34 citations in OpenAlex.
- Kinetic mechanisms for the sequence dependence of transcriptional errors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Spatially coordinated collective phosphorylation filters spatiotemporal noises for precise circadian timekeeping.iScience · 2023Article
- Auto-segmentation and time-dependent systematic analysis of mesoscale cellular structure in β-cells during insulin secretion.PloS one · 2022Article
- Using soft X-ray tomography for rapid whole-cell quantitative imaging of SARS-CoV-2-infected cells.Cell reports methods · 2021Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
For a chemical signal to propagate across a cell, it must navigate a tortuous environment involving a variety of organelle barriers. In this work we study mathematical models for a basic chemical signal, the arrival times at the nuclear membrane of proteins that are activated at the cell membrane and diffuse throughout the cytosol. Organelle surfaces within human B cells are reconstructed from soft X-ray tomographic images, and modeled as reflecting barriers to the molecules' diffusion. We show that signal inactivation sharpens signals, reducing variability in the arrival time at the nuclear membrane. Inactivation can also compensate for an observed slowdown in signal propagation induced by the presence of organelle barriers, leading to arrival times at the nuclear membrane that are comparable to models in which the cytosol is treated as an open, empty region. In the limit of strong signal inactivation this is achieved by filtering out molecules that traverse non-geodesic paths.
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