Gene families expand by gene duplication, and resulting paralogs diverge through mutation. Functional diversification can include neofunctionalization as well as subfunctionalization of ancestral functions. In addition, redundancy in which multiple genes fulfill overlapping functions is often maintained. Here, we use the family of 40 Caenorhabditis elegans insulins to gain insight into the balance between specificity and redundancy. The insulin/insulin-like growth factor (IIS) pathway comprises a single receptor, DAF-2. To date, no single insulin-like peptide recapitulates all DAF-2-associated phenotypes, likely due to redundancy between insulin-like genes. To provide a first-level annotation of potential patterns of redundancy, we comprehensively delineate the spatiotemporal and conditional expression of all 40 insulins in living animals. We observe extensive dynamics in expression that can explain the lack of simple patterns of pairwise redundancy. We propose a model in which gene families evolve to attain differential alliances in different tissues and in response to a range of environmental stresses.
%0 Journal Article
%1 Ritter2013Complex
%A Ritter, Ashlyn D.
%A Shen, Yuan
%A Fuxman Bass, Juan
%A Jeyaraj, Sankarganesh
%A Deplancke, Bart
%A Mukhopadhyay, Arnab
%A Xu, Jian
%A Driscoll, Monica
%A Tissenbaum, Heidi A.
%A Walhout, Albertha J.
%D 2013
%J Genome research
%K dynamics gene-expression robustness
%N 6
%P 954--965
%R 10.1101/gr.150466.112
%T Complex expression dynamics and robustness in C. elegans insulin networks.
%U http://dx.doi.org/10.1101/gr.150466.112
%V 23
%X Gene families expand by gene duplication, and resulting paralogs diverge through mutation. Functional diversification can include neofunctionalization as well as subfunctionalization of ancestral functions. In addition, redundancy in which multiple genes fulfill overlapping functions is often maintained. Here, we use the family of 40 Caenorhabditis elegans insulins to gain insight into the balance between specificity and redundancy. The insulin/insulin-like growth factor (IIS) pathway comprises a single receptor, DAF-2. To date, no single insulin-like peptide recapitulates all DAF-2-associated phenotypes, likely due to redundancy between insulin-like genes. To provide a first-level annotation of potential patterns of redundancy, we comprehensively delineate the spatiotemporal and conditional expression of all 40 insulins in living animals. We observe extensive dynamics in expression that can explain the lack of simple patterns of pairwise redundancy. We propose a model in which gene families evolve to attain differential alliances in different tissues and in response to a range of environmental stresses.
@article{Ritter2013Complex,
abstract = {
Gene families expand by gene duplication, and resulting paralogs diverge through mutation. Functional diversification can include neofunctionalization as well as subfunctionalization of ancestral functions. In addition, redundancy in which multiple genes fulfill overlapping functions is often maintained. Here, we use the family of 40 Caenorhabditis elegans insulins to gain insight into the balance between specificity and redundancy. The insulin/insulin-like growth factor ({IIS}) pathway comprises a single receptor, {DAF}-2. To date, no single insulin-like peptide recapitulates all {DAF}-2-associated phenotypes, likely due to redundancy between insulin-like genes. To provide a first-level annotation of potential patterns of redundancy, we comprehensively delineate the spatiotemporal and conditional expression of all 40 insulins in living animals. We observe extensive dynamics in expression that can explain the lack of simple patterns of pairwise redundancy. We propose a model in which gene families evolve to attain differential alliances in different tissues and in response to a range of environmental stresses.
},
added-at = {2018-12-02T16:09:07.000+0100},
author = {Ritter, Ashlyn D. and Shen, Yuan and Fuxman Bass, Juan and Jeyaraj, Sankarganesh and Deplancke, Bart and Mukhopadhyay, Arnab and Xu, Jian and Driscoll, Monica and Tissenbaum, Heidi A. and Walhout, Albertha J.},
biburl = {https://www.bibsonomy.org/bibtex/28835e3c31e19ae787cd568eef759b8cf/karthikraman},
citeulike-article-id = {12749692},
citeulike-linkout-0 = {http://dx.doi.org/10.1101/gr.150466.112},
citeulike-linkout-1 = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3668363/},
citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/23539137},
citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=23539137},
doi = {10.1101/gr.150466.112},
interhash = {c092b2fbb4a07b494bf967c78b009199},
intrahash = {8835e3c31e19ae787cd568eef759b8cf},
issn = {1549-5469},
journal = {Genome research},
keywords = {dynamics gene-expression robustness},
month = jun,
number = 6,
pages = {954--965},
pmcid = {PMC3668363},
pmid = {23539137},
posted-at = {2013-11-04 07:21:47},
priority = {2},
timestamp = {2018-12-02T16:09:07.000+0100},
title = {Complex expression dynamics and robustness in C. elegans insulin networks.},
url = {http://dx.doi.org/10.1101/gr.150466.112},
volume = 23,
year = 2013
}