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Dev Biol. 2013 May 1;377(1):305-17. doi: 10.1016/j.ydbio.2013.01.010. Epub 2013 Jan 18.

Lack of tailless leads to an increase in expression variability in Drosophila embryos.

Author information

  • 1EMBL/CRG Research Unit in Systems Biology, CRG-Centre de Regulació Genòmica, and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain.

Erratum in

  • Dev Biol. 2013 May 1;377(1):318.

Abstract

Developmental processes are robust, or canalised: dynamic patterns of gene expression across space and time are regulated reliably and precisely in the presence of genetic and environmental perturbations. It remains unclear whether canalisation relies on specific regulatory factors (such as heat-shock proteins), or whether it is based on more general redundancy and distributed robustness at the network level. The latter explanation implies that mutations in many regulatory factors should exhibit loss of canalisation. Here, we present a quantitative characterisation of segmentation gene expression patterns in mutants of the terminal gap gene tailless (tll) in Drosophila melanogaster. Our analysis provides new insights into the dynamic mechanisms underlying gap gene regulation, and reveals significantly increased variability of gene expression in the mutant compared to the wild-type background. We show that both position and timing of posterior segmentation gene expression domains vary strongly from embryo-to-embryo in tll mutants. This variability must be caused by a vulnerability in the regulatory system which is hidden or buffered in the wild-type, but becomes uncovered by the deletion of tll. Our analysis provides evidence that loss of canalisation in mutants could be more widespread than previously thought.

Copyright © 2013 Elsevier Inc. All rights reserved.

PMID:
23333944
[PubMed - indexed for MEDLINE]
PMCID:
PMC3635121
Free PMC Article
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