ArticleGenetics2000
Genetic analysis of a Y-chromosome region that induces triplosterile phenotypes and is essential for spermatid individualization in Drosophila melanogaster.
Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Fitness consequences of sex chromosome aneuploidy in Drosophila melanogaster.PLoS genetics · 2025Article
- Ribosomal DNA Instability as a Potential Cause of Karyotype Evolution.Molecular biology and evolution · 2022Article
- Combover interacts with the axonemal component Rsp3 and is required forDevelopment (Cambridge, England) · 2019Article
- Satellite DNA-containing gigantic introns in a unique gene expression program during Drosophila spermatogenesis.PLoS genetics · 2019Article
- Article
- A young Drosophila duplicate gene plays essential roles in spermatogenesis by regulating several Y-linked male fertility genes.PLoS genetics · 2010Article
- The hsp60B gene of Drosophila melanogaster is essential for the spermatid individualization process.Cell stress & chaperones · 2001Article
- Y chromosomal fertility factors kl-2 and kl-3 of Drosophila melanogaster encode dynein heavy chain polypeptides.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Separating from the pack: Molecular mechanisms ofSpermatogenesisArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterochromatic Y chromosome of Drosophila melanogaster contains approximately 40 Mb of DNA but has only six loci mutable to male sterility. Region h1-h9 on YL, which carries the kl-3 and kl-5 loci, induces male sterility when present in three copies. We show that three separate segments within the region are responsible for the triplosterility and have an additive effect on male fertility. The triplosterile males displayed pleiotropic defects, beginning at early postmeiotic stages. However, the triplosterility was unaffected by kl-3 or kl-5 alleles. These data suggest that region h1-h9 is complex and may contain novel functions in addition to those of the previously identified kl-3 and kl-5 loci. The kl-3 and kl-5 mutations as well as deficiencies within region h1-h9 result in loss of the spermatid axonemal outer dynein arms. Examination using fluorescent probes showed that males deficient for h1-h3 or h4-h9 displayed a postmeiotic lesion with disrupted individualization complexes scattered along the spermatid bundle. In contrast, the kl-3 and kl-5 mutations had no effect on spermatid individualization despite the defect in the axonemes. These results demonstrate that region h1-h9 carries genetically separable functions: one required for spermatid individualization and the other essential for assembling the axonemal dynein arms.
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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.