ArticleDevelopment (Cambridge, England)2003
Even-skipped, acting as a repressor, regulates axonal projections in Drosophila.
Article in Development (Cambridge, England), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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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
92 citing papers in PubMed, 147 citations in OpenAlex.
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- Hunchback activates Bicoid in Pair1 neurons to regulate synapse number and locomotor circuit function.Current biology : CB · 2022Article
- Dissection and Direct Imaging of Axonal Transport in Drosophila Segmental Nerves.Methods in molecular biology (Clifton, N.J.) · 2022Article
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- Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Retrograde Tracing of Drosophila Embryonic Motor Neurons Using Lipophilic Fluorescent Dyes.Journal of visualized experiments : JoVE · 2020Article
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- Regulation of forward and backward locomotion through intersegmental feedback circuits in Drosophila larvae.Nature communications · 2019Article
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- An ancient role for collier/Olf/Ebf (COE)-type transcription factors in axial motor neuron development.Neural development · 2019Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Nervous system-specific eve mutants were created by removing regulatory elements from a 16 kb transgene capable of complete rescue of normal eve function. When transgenes lacking the regulatory element for either RP2+a/pCC, EL or U/CQ neurons were placed in an eve-null background, eve expression was completely eliminated in the corresponding neurons, without affecting other aspects of eve expression. Many of these transgenic flies were able to survive to fertile adulthood. In the RP2+a/pCC mutant flies: (1) both RP2 and aCC showed abnormal axonal projection patterns, failing to innervate their normal target muscles; (2) the cell bodies of these neurons were positioned abnormally; and (3) in contrast to the wild type, pCC axons often crossed the midline. The Eve HD alone was able to provide a weak, partial rescue of the mutant phenotype, while both the Groucho-dependent and -independent repressor domains contributed equally to full rescue of each aspect of the mutant phenotype. Complete rescue was also obtained with a chimeric protein containing the Eve HD and the Engrailed repressor domain. Consistent with the apparent sufficiency of repressor function, a fusion protein between the Gal4 DNA-binding domain and Eve repressor domains was capable of actively repressing UAS target genes in these neurons. A key target of the repressor function of Eve was Drosophila Hb9, the derepression of which correlated with the mutant phenotype in individual eve-mutant neurons. Finally, homologues of Eve from diverse species were able to rescue the eve mutant phenotype, indicating conservation of both targeting and repression functions in the nervous system.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.