ArticleGenetics2007
Antagonizing scalloped with a novel vestigial construct reveals an important role for scalloped in Drosophila melanogaster leg, eye and optic lobe development.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Polycomb safeguards imaginal disc specification through control of the Vestigial-Scalloped complex.bioRxiv : the preprint server for biology · 2023Article
- Immune function analysis ofFrontiers in physiology · 2022Article
- Identification of a classical bipartite nuclear localization signal in the Drosophila TEA/ATTS protein scalloped.PloS one · 2011Article
- Vestigial is required during late-stage muscle differentiation in Drosophila melanogaster embryos.Molecular biology of the cell · 2010Article
- A regulatory code for neuron-specific odor receptor expression.PLoS biology · 2008Article
- Redundant roles of Tead1 and Tead2 in notochord development and the regulation of cell proliferation and survival.Molecular and cellular biology · 2008Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scalloped (SD), a TEA/ATTS-domain-containing protein, is required for the proper development of Drosophila melanogaster. Despite being expressed in a variety of tissues, most of the work on SD has been restricted to understanding its role and function in patterning the adult wing. To gain a better understanding of its role in development, we generated sd(47M) flip-in mitotic clones. The mitotic clones had developmental defects in the leg and eye. Further, by removing the VG domains involved in activation, we created a reagent (VGDeltaACT) that disrupts the ability of SD to form a functional transcription factor complex and produced similar phenotypes to the flip-in mitotic clones. The VGDeltaACT construct also disrupted adult CNS development. Expression of the VGDeltaACT construct in the wing alters the cellular localization of VG and produces a mutant phenotype, indicating that the construct is able to antagonize the normal function of the SD/VG complex. Expression of the protein:protein interaction portion of SD is also able to elicit similar phenotypes, suggesting that SD interacts with other cofactors in the leg, eye, and adult CNS. Furthermore, antagonizing SD in larval tissues results in cell death, indicating that SD may also have a role in cell survival.
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Registered trials
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