Cargando…
Why and how genetic canalization evolves in gene regulatory networks
BACKGROUND: Genetic canalization reflects the capacity of an organism’s phenotype to remain unchanged in spite of mutations. As selection on genetic canalization is weak and indirect, whether or not genetic canalization can reasonably evolve in complex genetic architectures is still an open question...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5100197/ https://www.ncbi.nlm.nih.gov/pubmed/27821071 http://dx.doi.org/10.1186/s12862-016-0801-2 |
_version_ | 1782466091421794304 |
---|---|
author | Rünneburger, Estelle Le Rouzic, Arnaud |
author_facet | Rünneburger, Estelle Le Rouzic, Arnaud |
author_sort | Rünneburger, Estelle |
collection | PubMed |
description | BACKGROUND: Genetic canalization reflects the capacity of an organism’s phenotype to remain unchanged in spite of mutations. As selection on genetic canalization is weak and indirect, whether or not genetic canalization can reasonably evolve in complex genetic architectures is still an open question. In this paper, we use a quantitative model of gene regulatory network to describe the conditions in which substantial canalization is expected to emerge in a stable environment. RESULTS: Through an individual-based simulation framework, we confirmed that most parameters associated with the network topology (complexity and size of the network) have less influence than mutational parameters (rate and size of mutations) on the evolution of genetic canalization. We also established that selecting for extreme phenotypic optima (nil or full gene expression) leads to much higher canalization levels than selecting for intermediate expression levels. Overall, constrained networks evolve less canalization than networks in which some genes could evolve freely (i.e. without direct stabilizing selection pressure on gene expression). CONCLUSIONS: Taken together, these results lead us to propose a two-fold mechanism involved in the evolution of genetic canalization in gene regulatory networks: the shrinkage of mutational target (useless genes are virtually removed from the network) and redundancy in gene regulation (so that some regulatory factors can be lost without affecting gene expression). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12862-016-0801-2) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5100197 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-51001972016-11-08 Why and how genetic canalization evolves in gene regulatory networks Rünneburger, Estelle Le Rouzic, Arnaud BMC Evol Biol Research Article BACKGROUND: Genetic canalization reflects the capacity of an organism’s phenotype to remain unchanged in spite of mutations. As selection on genetic canalization is weak and indirect, whether or not genetic canalization can reasonably evolve in complex genetic architectures is still an open question. In this paper, we use a quantitative model of gene regulatory network to describe the conditions in which substantial canalization is expected to emerge in a stable environment. RESULTS: Through an individual-based simulation framework, we confirmed that most parameters associated with the network topology (complexity and size of the network) have less influence than mutational parameters (rate and size of mutations) on the evolution of genetic canalization. We also established that selecting for extreme phenotypic optima (nil or full gene expression) leads to much higher canalization levels than selecting for intermediate expression levels. Overall, constrained networks evolve less canalization than networks in which some genes could evolve freely (i.e. without direct stabilizing selection pressure on gene expression). CONCLUSIONS: Taken together, these results lead us to propose a two-fold mechanism involved in the evolution of genetic canalization in gene regulatory networks: the shrinkage of mutational target (useless genes are virtually removed from the network) and redundancy in gene regulation (so that some regulatory factors can be lost without affecting gene expression). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12862-016-0801-2) contains supplementary material, which is available to authorized users. BioMed Central 2016-11-08 /pmc/articles/PMC5100197/ /pubmed/27821071 http://dx.doi.org/10.1186/s12862-016-0801-2 Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Rünneburger, Estelle Le Rouzic, Arnaud Why and how genetic canalization evolves in gene regulatory networks |
title | Why and how genetic canalization evolves in gene regulatory networks |
title_full | Why and how genetic canalization evolves in gene regulatory networks |
title_fullStr | Why and how genetic canalization evolves in gene regulatory networks |
title_full_unstemmed | Why and how genetic canalization evolves in gene regulatory networks |
title_short | Why and how genetic canalization evolves in gene regulatory networks |
title_sort | why and how genetic canalization evolves in gene regulatory networks |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5100197/ https://www.ncbi.nlm.nih.gov/pubmed/27821071 http://dx.doi.org/10.1186/s12862-016-0801-2 |
work_keys_str_mv | AT runneburgerestelle whyandhowgeneticcanalizationevolvesingeneregulatorynetworks AT lerouzicarnaud whyandhowgeneticcanalizationevolvesingeneregulatorynetworks |