title: Lack of tailless leads to an increase in expression variability in Drosophila embryos.
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.
authors: EMBL/CRG Research Unit in Systems Biology, CRG-Centre de Regulació Genòmica, and Universitat Pompeu Fabra (UPF), Dr. Aiguader 88, 08003 Barcelona, Spain.
authors: Hilde
authors: H
authors: Janssens
authors: Anton
authors: A
authors: Crombach
authors: Karl Richard
authors: KR
authors: Wotton
authors: Damjan
authors: D
authors: Cicin-Sain
authors: Svetlana
authors: S
authors: Surkova
authors: Chea Lu
authors: CL
authors: Lim
authors: Maria
authors: M
authors: Samsonova
authors: Michael
authors: M
authors: Akam
authors: Johannes
authors: J
authors: Jaeger
mesh_terms: D000818:Animals; D001756:Blastoderm / Q000166:cytology / Q000378:metabolism; D019521:Body Patterning / Q000235:genetics; D029721:Drosophila Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D004331:Drosophila melanogaster / Q000196:embryology* / Q000235:genetics*; D004625:Embryo, Nonmammalian / Q000166:cytology / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D053263:Gene Regulatory Networks / Q000235:genetics; D017344:Genes, Insect / Q000235:genetics; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D012097:Repressor Proteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D029721:Drosophila Proteins; D018398:Homeodomain Proteins; D012097:Repressor Proteins; C074090:TLL protein, Drosophila; D014157:Transcription Factors; C052837:eve protein, Drosophila