ArticleGenetics1995
A screen for modifiers of Deformed function in Drosophila.
Article in Genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 32 citations in OpenAlex.
- Epigenetic inheritance and gene expression regulation in early Drosophila embryos.EMBO reports · 2024Review
- Polycomb and Trithorax Group Genes inGenetics · 2017Review
- Mechanisms and functions of Nrf2 signaling in Drosophila.Free radical biology & medicine · 2015Review
- A screen for genes that interact with the Drosophila pair-rule segmentation gene fushi tarazu.Genetics · 2004Article
- A green fluorescent protein reporter genetic screen that identifies modifiers of Hox gene function in the Drosophila embryo.Genetics · 2002Article
- A genetic screen of the Drosophila X chromosome for mutations that modify Deformed function.Genetics · 1998Article
- A model for extradenticle function as a switch that changes HOX proteins from repressors to activators.The EMBO journal · 1997Article
- Drosophotoxicology: the growing potential for Drosophila in neurotoxicology.Neurotoxicology and teratologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proteins produced by the homeotic genes of the Hox family assign different identifies to cells on the anterior/posterior axis. Relatively little is known about the signalling pathways that modulate their activities or the factors with which they interact to assign specific segmental identifies. To identify genes that might encode such functions, we performed a screen for second site mutations that reduce the viability of animals carrying hypomorphic mutant alleles of the Drosophila homeotic locus, Deformed. Genes mapping to six complementation groups on the third chromosome were isolated as modifiers of Deformed function. Products of two of these genes, sallimus and moira, have been previously proposed as homeotic activators since they suppress the dominant adult phenotype of Polycomb mutants. Mutations in hedgehog, which encodes secreted signalling proteins, were also isolated as Deformed loss-of-function enhancers. Hedgehog mutant alleles also suppress the Polycomb phenotype. Mutations were also isolated in a few genes that interact with Deformed but not with Polycomb, indicating that the screen identified genes that are not general homeotic activators. Two of these genes, cap 'n' collar and defaced, have defects in embryonic head development that are similar to defects seen in loss of function Deformed mutants.
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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.