ArticleG3 (Bethesda, Md.)2011
polo Is Identified as a Suppressor of bubR1 Nondisjunction in a Deficiency Screen of the Third Chromosome in Drosophila melanogaster.
Article in G3 (Bethesda, Md.), 2011. 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.
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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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Female Meiosis: Synapsis, Recombination, and Segregation inGenetics · 2018Review
- unfulfilled interacting genes display branch-specific roles in the development of mushroom body axons in Drosophila melanogaster.G3 (Bethesda, Md.) · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously characterized an EMS-induced allele of the bubR1 gene (bubR1(D1326N)) that separates the two functions of BubR1, causing meiotic nondisjunction but retaining spindle assembly checkpoint activity during somatic cell division in Drosophila melanogaster. Using this allele, we demonstrate that bubR1 meiotic nondisjunction is dosage sensitive, occurs for both exchange and nonexchange homologous chromosomes, and is associated with decreased maintenance of sister chromatid cohesion and of the synaptonemal complex during prophase I progression. We took advantage of these features to perform a genetic screen designed to identify third chromosome deficiencies having a dominant effect on bubR1(D1326N)/bubR1(rev1) meiotic phenotypes. We tested 65 deficiencies covering 60% of the third chromosome euchromatin. Among them, we characterized 24 deficiencies having a dominant effect on bubR1(D1326N)/bubR1(rev1) meiotic phenotypes that we classified in two groups: (1) suppressor of nondisjunction and (2) enhancer of nondisjunction. Among these 24 deficiencies, our results show that deficiencies uncovering the polo locus act as suppressor of bubR1 nondisjunction by delaying meiotic prophase I progression and restoring chiasmata formation as observed by the loading of the condensin subunit SMC2. Furthermore, we identified two deficiencies inducing a lethal phenotype during embryonic development and thus affecting BubR1 kinase activity in somatic cells and one deficiency causing female sterility. Overall, our genetic screening strategy proved to be highly sensitive for the identification of modifiers of BubR1 kinase activity in both meiosis and mitosis.
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Registered trials
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