Complex expression dynamics and robustness in C. elegans insulin networks
- Ashlyn D. Ritter1,
- Yuan Shen1,
- Juan Fuxman Bass1,
- Sankarganesh Jeyaraj1,
- Bart Deplancke1,
- Arnab Mukhopadjay1,
- Jian Xu2,
- Monica Driscoll2,
- Heidi A. Tissenbaum1 and
- Albertha J.M. Walhout1,3
- ↵* Corresponding author; email: marian.walhout{at}umassmed.edu
Abstract
Gene families expand by gene duplication and resulting paralogs diverge through mutation. Functional diversification can include neo-functionalization as well as sub-functionalization 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 pair-wise 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.
- Received October 9, 2012.
- Accepted March 22, 2013.
- © 2013, Published by Cold Spring Harbor Laboratory Press
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