ArticleChromosoma2020
shani mutation in mouse affects splicing of Spata22 and leads to impaired meiotic recombination.
Article in Chromosoma, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Critical roles of MCM8 in meiotic recombination during mouse spermatogenesis.bioRxiv : the preprint server for biology · 2026Article
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
- Intercellular bridges are essential for transposon repression and meiosis in the male germline.Nature communications · 2025Article
- Genetic variants underlying spermatogenic arrests in men with non-obstructive azoospermia.Cell cycle (Georgetown, Tex.) · 2023Article
- Pathogenic variants in the human m6A reader YTHDC2 are associated with primary ovarian insufficiency.JCI insight · 2022Article
- yama, a mutant allele of Mov10l1, disrupts retrotransposon silencing and piRNA biogenesis.PLoS genetics · 2021Article
- The ssDNA-binding protein MEIOB acts as a dosage-sensitive regulator of meiotic recombination.Nucleic acids research · 2020Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Recombination is crucial for chromosome pairing and segregation during meiosis. SPATA22, along with its direct binding partner and functional collaborator, MEIOB, is essential for the proper repair of double-strand breaks (DSBs) during meiotic recombination. Here, we describe a novel point-mutated allele (shani) of mouse Spata22 that we isolated in a forward genetic screen. shani mutant mice phenocopy Spata22-null and Meiob-null mice: mutant cells appear to form DSBs and initiate meiotic recombination, but are unable to complete DSB repair, leading to meiotic prophase arrest, apoptosis and sterility. shani mutants show precocious loss of DMC1 foci and improper accumulation of BLM-positive recombination foci, reinforcing the requirement of SPATA22-MEIOB for the proper progression of meiotic recombination events. The shani mutation lies within a Spata22 coding exon and molecular characterization shows that it leads to incorrect splicing of the Spata22 mRNA, ultimately resulting in no detectable SPATA22 protein. We propose that the shani mutation alters an exonic splicing enhancer element (ESE) within the Spata22 transcript. The affected DNA nucleotide is conserved in most tetrapods examined, suggesting that the splicing regulation we describe here may be a conserved feature of Spata22 regulation.
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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.