ArticleGenetics2023
Caenorhabditis elegans spermatocytes can segregate achiasmate homologous chromosomes apart at higher than random frequency during meiosis I.
Article in Genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Multifaceted and evolutionarily dynamic interactions betweenbioRxiv : the preprint server for biology · 2026Article
- Remote homology and functional genetics unmask deeply preserved Scm3/HJURP orthologs in metazoans.Science advances · 2026Article
- Remote homology and functional genetics unmask deeply preserved Scm3/HJURP orthologs in metazoans.bioRxiv : the preprint server for biology · 2026Article
- Loss of meiotic double strand breaks triggers recruitment of recombination-independent pro-crossover factors in C. elegans spermatogenesis.PLoS genetics · 2025Article
- Exclusion of the endoplasmic reticulum from themicroPublication biology · 2025Article
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Chromosome segregation errors during meiosis are the leading cause of aneuploidy. Faithful chromosome segregation during meiosis in most eukaryotes requires a crossover which provides a physical attachment holding homologs together in a "bivalent." Crossovers are critical for homologs to be properly aligned and partitioned in the first meiotic division. Without a crossover, individual homologs (univalents) might segregate randomly, resulting in aneuploid progeny. However, Caenorhabditis elegans zim-2 mutants, which have crossover defects on chromosome V, have fewer dead embryos than that expected from random segregation. This deviation from random segregation is more pronounced in zim-2 males than that in females. We found three phenomena that can explain this apparent discrepancy. First, we detected crossovers on chromosome V in both zim-2(tm574) oocytes and spermatocytes, suggesting a redundant mechanism to make up for the ZIM-2 loss. Second, after accounting for the background crossover frequency, spermatocytes produced significantly more euploid gametes than what would be expected from random segregation. Lastly, trisomy of chromosome V is viable and fertile. Together, these three phenomena allow zim-2(tm574) mutants with reduced crossovers on chromosome V to have more viable progeny. Furthermore, live imaging of meiosis in spo-11(me44) oocytes and spermatocytes, which exhibit crossover failure on all 6 chromosomes, showed 12 univalents segregating apart in roughly equal masses in a homology-independent manner, supporting the existence of a mechanism that segregates any 2 chromosomes apart.
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