ArticlePloS one2011
Tramtrack is genetically upstream of genes controlling tracheal tube size in Drosophila.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- The black honey bee genome: insights on specific structural elements and a first step towards pangenomes.Genetics, selection, evolution : GSE · 2024Article
- Structure of the N-terminal domain of the protein Expansion: an 'Expansion' to the Smad MH2 fold.Acta crystallographica. Section D, Biological crystallography · 2015Article
- Deciphering the genetic programme triggering timely and spatially-regulated chitin deposition.PLoS genetics · 2015Article
- Coordinated repression and activation of two transcriptional programs stabilizes cell fate during myogenesis.Development (Cambridge, England) · 2014Article
- Following the 'tracks': Tramtrack69 regulates epithelial tube expansion in the Drosophila ovary through Paxillin, Dynamin, and the homeobox protein Mirror.Developmental biology · 2013Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The Drosophila transcription factor Tramtrack (Ttk) is involved in a wide range of developmental decisions, ranging from early embryonic patterning to differentiation processes in organogenesis. Given the wide spectrum of functions and pleiotropic effects that hinder a comprehensive characterisation, many of the tissue specific functions of this transcription factor are only poorly understood. We recently discovered multiple roles of Ttk in the development of the tracheal system on the morphogenetic level. Here, we sought to identify some of the underlying genetic components that are responsible for the tracheal phenotypes of Ttk mutants. We therefore profiled gene expression changes after Ttk loss- and gain-of-function in whole embryos and cell populations enriched for tracheal cells. The analysis of the transcriptomes revealed widespread changes in gene expression. Interestingly, one of the most prominent gene classes that showed significant opposing responses to loss- and gain-of-function was annotated with functions in chitin metabolism, along with additional genes that are linked to cellular responses, which are impaired in ttk mutants. The expression changes of these genes were validated by quantitative real-time PCR and further functional analysis of these candidate genes and other genes also expected to control tracheal tube size revealed at least a partial explanation of Ttk's role in tube size regulation. The computational analysis of our tissue-specific gene expression data highlighted the sensitivity of the approach and revealed an interesting set of novel putatively tracheal genes.
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