ArticleGenetica1996
Genetic and molecular analysis of a set of unstable white mutants in Drosophila melanogaster.
Article in Genetica, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 5 citations in OpenAlex.
- In vivo analysis of Drosophila SU(Z)12 function.Molecular genetics and genomics : MGG · 2008Article
- An FB-NOF mediated duplication of the white gene is responsible for the zeste1 phenotype in some Drosophila melanogaster unstable strains.Molecular genetics and genomics : MGG · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two related unstable mutants at the white locus of Drosophila melanogaster show different interactions with the zeste1 mutant: one mutated white gene becomes repressed in males, whereas the other is unaffected by z1. By use of Southern blot techniques and by constructing genomic lambda-libraries, molecular analyses of the white regions of these two strains were performed. The results showed a single difference at a site 2.5 kb (kilobases) downstream of the white transcription unit. In both strains, FB (foldback) elements were integrated at this site, but the repressed strain also harboured a 4 kb NOF (Nofretete) element. No other restriction site polymorphisms between the two strains were observed within a 120 kb region surrounding the white gene. The extent of twelve white deletions and twelve white transpositions deriving from these unstable strains was analysed by in situ hybridisation and Southern blot techniques. The results revealed that the distal breakpoint of all aberrations coincided with the insertion site of the mobile elements, but that the centromere proximal breakpoints varied. The mechanisms for the instability and the interaction with the zeste1 mutant are discussed.
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Registered trials
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