ArticleScientific reports2020
Reverse genetics reveals single gene of every candidate on Hybrid sterility, X Chromosome QTL 2 (Hstx2) are dispensable for spermatogenesis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- Mouse X-linked microRNA cluster regulates the meiotic checkpoint andProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Regional random mutagenesis driven by multiple sgRNAs and diverse on-target genome editing events to identify functionally important elements in non-coding regions.Open biology · 2024Article
- Meiotic Recognition of Evolutionarily Diverged Homologs: Chromosomal Hybrid Sterility Revisited.Molecular biology and evolution · 2023Article
- On the impermanence of species: The collapse of genetic incompatibilities in hybridizing populations.Evolution; international journal of organic evolution · 2022Article
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13 authors.
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Abstract
F1 hybrid progenies between related subspecies often show hybrid sterility (HS) or inviability. HS is caused by failure of meiotic chromosome synapsis and sex body formation in house mouse. Previous studies identified two HS critical genomic regions named Hstx2 on Chr X and Hst1 on Chr 17 by murine forward genetic approaches. HS gene on Hst1 was reported to be Prdm9. Intersubspecific polymorphisms of Prdm9 induce HS in hybrids, and Prdm9 null mutation leads to sterility in the inbred strain. However, HS gene on Hstx2 remains unknown. Here, using knock-out studies, we showed that HS candidate genes on Hstx2 are not individually essential for spermatogenesis in B6 strain. We examined 12 genes on Hstx2: Ctag2, 4930447F04Rik, Mir743, Mir465d, Mir465c-2, Mir465b-1, Mir465c-1, Mir465, Gm1140, Gm14692, 4933436I01Rik, and Gm6812. These genes were expressed in adult testes, and showed intersubspecific polymorphisms on expressed regions. This first reverse genetic approach to identify HS gene on Hstx2 suggested that the loss of function of any one HS candidate gene does not cause complete sterility, unlike Prdm9. Thus, the mechanism(s) of HS by the HS gene on Hstx2 might be different from that of Prdm9.
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