Metazoan operons accelerate recovery from growth-arrested states.

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2011-06-10

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Abstract

Existing theories explain why operons are advantageous in prokaryotes, but their occurrence in metazoans is an enigma. Nematode operon genes, typically consisting of growth genes, are significantly upregulated during recovery from growth-arrested states. This expression pattern is anticorrelated to nonoperon genes, consistent with a competition for transcriptional resources. We find that transcriptional resources are initially limiting during recovery and that recovering animals are highly sensitive to any additional decrease in transcriptional resources. We provide evidence that operons become advantageous because, by clustering growth genes into operons, fewer promoters compete for the limited transcriptional machinery, effectively increasing the concentration of transcriptional resources and accelerating recovery. Mathematical modeling reveals how a moderate increase in transcriptional resources can substantially enhance transcription rate and recovery. This design principle occurs in different nematodes and the chordate C. intestinalis. As transition from arrest to rapid growth is shared by many metazoans, operons could have evolved to facilitate these processes.

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Published Version (Please cite this version)

10.1016/j.cell.2011.05.013

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Zaslaver, Alon, L Ryan Baugh and Paul W Sternberg (2011). Metazoan operons accelerate recovery from growth-arrested states. Cell, 145(6). pp. 981–992. 10.1016/j.cell.2011.05.013 Retrieved from https://hdl.handle.net/10161/10403.

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Scholars@Duke

Baugh

L. Ryan Baugh

Professor of Biology

The Baugh Lab is interested in phenotypic plasticity and physiological adaptation to variable environmental conditions. We are using the roundworm C. elegans to understand how animals adapt to starvation using primarily genetic and genomic approaches. We are studying how development is governed by nutrient availability, how animals survive starvation, and the long-term consequences of starvation including adult disease and transgenerational epigenetic inheritance.


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