ArticleGenetics1997
Beaded of Goldschmidt, an antimorphic allele of Serrate, encodes a protein lacking transmembrane and intracellular domains.
Article in Genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Drosophila Rabex-5 restricts Notch activity in hematopoietic cells and maintains hematopoietic homeostasis.Journal of cell science · 2015Article
- An extracellular region of Serrate is essential for ligand-induced cis-inhibition of Notch signaling.Development (Cambridge, England) · 2013Article
- Endothelial cells promote the colorectal cancer stem cell phenotype through a soluble form of Jagged-1.Cancer cell · 2013Article
- Review
- Two distinct mechanisms segregate Prospero in the longitudinal glia underlying the timing of interactions with axons.Neuron glia biology · 2007Article
- A genetic screen for novel components of the notch signaling pathway during Drosophila bristle development.Genetics · 1998Article
- The Rap1 small GTPase affects cell fate or survival and morphogenetic patterning during Drosophila melanogaster eye development.Differentiation; research in biological diversityArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Serrate (Ser) is an essential gene in Drosophila melanogaster best known for the Ser dominant (SerD) allele and its effects on wing development. Animals heterozygous or homozygous for SerD are viable and exhibit loss of wing margin tissue and associated bristles and hairs. The Beaded of Goldschmidt (BdG) allele of Ser, when heterozygous to wild type, will also produce animals exhibiting loss of wing margin material. However, animals homozygous for BdG exhibit a larval lethal phenotype comparable to animals homozygous for loss-of-function Ser alleles. BdG is a partial duplication of the Ser locus with a single 5' Ser-homologous region and two distinct 3' regions. Meiotic recombination between BdG and a wild-type Ser chromosome demonstrated that only one DNA lesion, caused by the insertion of a transposable roo element into the coding regions of the Ser transcript, appears capable of generating BdG phenotypes. Due to the roo insertion, the protein product is predicted to be prematurely truncated and lack an extracellular cysteine-rich region along with the transmembrane and intracellular domains found within the normal SERRATE (SER) protein. The loss of these protein domains apparently contributes to the antimorphic nature of this mutation.
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Registered trials
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