ArticleMolecular genetics and genomics : MGG2004
Creation of EcR isoform-specific mutations in Drosophila melanogaster via local P element transposition, imprecise P element excision, and male recombination.
Article in Molecular genetics and genomics : MGG, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 16 citations in OpenAlex.
- Ultraspiracle-independent anti-apoptotic function of ecdysone receptors is required for the survival of larval peptidergic neurons via suppression of grim expression in Drosophila melanogaster.Apoptosis : an international journal on programmed cell death · 2019Article
- Identifying and characterising key alternative splicing events in Drosophila development.BMC genomics · 2015Article
- Isoform-specific regulation of a steroid hormone nuclear receptor by an E3 ubiquitin ligase in Drosophila melanogaster.Genetics · 2011Article
- Steroid-triggered, cell-autonomous death of a Drosophila motoneuron during metamorphosis.Neural development · 2011Article
- Article
- Phenotypic analysis of EcR-A mutants suggests that EcR isoforms have unique functions during Drosophila development.Developmental biology · 2005Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Collections of single P transposable-element insertion strains that currently inactivate more than 25% of essential Drosophila genes have proven to be a valuable tool for genome research in Drosophila melanogaster. For genes unrepresented in these collections, strategies including local P element transposition and transposase-induced imprecise excision can be used to inactivate or delete the gene of interest. Here we report our use of local P element transposition followed by imprecise P element excision and transposase-induced male recombination to generate two deficiencies specific for the EcR-A isoform of the ecdysone receptor ( EcR) gene, and four larger deficiencies likely to affect multiple EcR functions. We also report here the determination of sequences flanking six EcR-B deficiencies generated in a previous imprecise excision screen. EcR-A encodes one of a family of three related nuclear receptor proteins that, together with the heterodimer partner USP, mediate ecdysone signaling during Drosophila development. Our results delineate sequences required in vivo for EcR-A function, as well as identifying EcR-A intron 1 sequences that are not essential for EcR function.
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Registered trials
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