Boolean networks have been proposed as potentially useful models for genetic control. An important aspect of these networks is the stability of their dynamics in response to small perturbations. Previous approaches to stability have assumed uncorrelated random network structure. Real gene networks typically have nontrivial topology significantly different from the random network paradigm. To address such situations, we present a general method for determining the stability of large Boolean networks of any specified network topology and predicting their steady-state behavior in response to small perturbations. Additionally, we generalize to the case where individual genes have a distribution of ” expression biases,” and we consider a nonsynchronous update, as well as extension of our method to non-Boolean models in which there are more than two possible gene states. We find that stability is governed by the maximum eigenvalue of a modified adjacency matrix, and we test this result by comparison with numerical simulations. We also discuss the possible application of our work to experimentally inferred gene networks.
%0 Journal Article
%1 Pomerance2009Effect
%A Pomerance, Andrew
%A Ott, Edward
%A Girvan, Michelle
%A Losert, Wolfgang
%D 2009
%J Proceedings of the National Academy of Sciences
%K boolean\_networks, cancer, genes, topology biological-networks
%N 20
%P 8209--8214
%R 10.1073/pnas.0900142106
%T The effect of network topology on the stability of discrete state models of genetic control
%U http://dx.doi.org/10.1073/pnas.0900142106
%V 106
%X Boolean networks have been proposed as potentially useful models for genetic control. An important aspect of these networks is the stability of their dynamics in response to small perturbations. Previous approaches to stability have assumed uncorrelated random network structure. Real gene networks typically have nontrivial topology significantly different from the random network paradigm. To address such situations, we present a general method for determining the stability of large Boolean networks of any specified network topology and predicting their steady-state behavior in response to small perturbations. Additionally, we generalize to the case where individual genes have a distribution of ” expression biases,” and we consider a nonsynchronous update, as well as extension of our method to non-Boolean models in which there are more than two possible gene states. We find that stability is governed by the maximum eigenvalue of a modified adjacency matrix, and we test this result by comparison with numerical simulations. We also discuss the possible application of our work to experimentally inferred gene networks.
@article{Pomerance2009Effect,
abstract = {{Boolean networks have been proposed as potentially useful models for genetic control. An important aspect of these networks is the stability of their dynamics in response to small perturbations. Previous approaches to stability have assumed uncorrelated random network structure. Real gene networks typically have nontrivial topology significantly different from the random network paradigm. To address such situations, we present a general method for determining the stability of large Boolean networks of any specified network topology and predicting their steady-state behavior in response to small perturbations. Additionally, we generalize to the case where individual genes have a distribution of ” expression biases,” and we consider a nonsynchronous update, as well as extension of our method to non-Boolean models in which there are more than two possible gene states. We find that stability is governed by the maximum eigenvalue of a modified adjacency matrix, and we test this result by comparison with numerical simulations. We also discuss the possible application of our work to experimentally inferred gene networks.}},
added-at = {2019-06-10T14:53:09.000+0200},
author = {Pomerance, Andrew and Ott, Edward and Girvan, Michelle and Losert, Wolfgang},
biburl = {https://www.bibsonomy.org/bibtex/2070625cd23d04f8da4ddee1b8afaefe7/nonancourt},
citeulike-article-id = {4563813},
citeulike-linkout-0 = {http://dx.doi.org/10.1073/pnas.0900142106},
citeulike-linkout-1 = {http://www.pnas.org/content/106/20/8209.short.abstract},
citeulike-linkout-2 = {http://www.pnas.org/content/106/20/8209.short.full.pdf},
citeulike-linkout-3 = {http://www.pnas.org/cgi/content/abstract/106/20/8209},
citeulike-linkout-4 = {http://view.ncbi.nlm.nih.gov/pubmed/19416903},
citeulike-linkout-5 = {http://www.hubmed.org/display.cgi?uids=19416903},
day = 19,
doi = {10.1073/pnas.0900142106},
interhash = {b756dfd357fee3e3dde695eab06bd383},
intrahash = {070625cd23d04f8da4ddee1b8afaefe7},
journal = {Proceedings of the National Academy of Sciences},
keywords = {boolean\_networks, cancer, genes, topology biological-networks},
month = may,
number = 20,
pages = {8209--8214},
pmid = {19416903},
posted-at = {2014-05-21 10:32:51},
priority = {2},
timestamp = {2019-07-31T13:50:37.000+0200},
title = {{The effect of network topology on the stability of discrete state models of genetic control}},
url = {http://dx.doi.org/10.1073/pnas.0900142106},
volume = 106,
year = 2009
}