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Updated: Mar 17, 2026
Dechorionation of Medaka Embryos and Cell Transplantation for the Generation of Chimeras
Published on: December 22, 2010
Disruption of dmc1 Produces Abnormal Sperm in Medaka (Oryzias latipes)
Ji Chen1, Xiaojuan Cui1, Shaoting Jia1,2
1State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, No. 7 Donghu South Road, Wuhan 430072, China.
Abstract:
DMC1 is a recombinase that is essential for meiotic synapsis. Experiments in extensive species of eukaryotes have indicated the independent role of DMC1 in repairing double strand breaks (DSBs) produced during meiosis I. Mutation of dmc1 in mice and human often leads to obstacles in spermatogenesis and male sterility. Here, we report on the disruption of dmc1 in male medaka (Oryzias latipes). Synapsis was disturbed in the mutant medaka testis nuclei, as observed in mice and other organisms. Unexpectedly, the mutant medaka could produce a few sperm and, although most of these had multiple tail or multiple head malformations, some of them could swim, and few of them even had insemination ability. Our transcriptome analysis showed that there was not a remarkable change in the expression of most of the genes involved in the pathways associated with the meiotic DNA repair and flagella assembly. Our results provided an indication of the accessory mechanisms that might be involved in the repair of DSBs during meiosis. In a species besides humans, we provided evidence that disorders in meiosis recombination might lead to the malformation of sperm.
Insights
Disrupting the DMC1 recombinase in medaka fish impaired meiotic synapsis but surprisingly allowed some sperm production. This suggests accessory mechanisms may aid double-strand break repair during meiosis.
Area of Science:
- Reproductive Biology
- Molecular Genetics
- Developmental Biology
Background:
- DMC1 is a crucial recombinase for meiotic synapsis and DNA repair in eukaryotes.
- Mutations in DMC1 are linked to spermatogenesis defects and male sterility in mammals.
- Understanding DMC1's role in non-mammalian species can reveal conserved and divergent mechanisms.
Purpose of the Study:
- To investigate the function of DMC1 in male medaka (Oryzias latipes).
- To analyze the consequences of DMC1 disruption on meiotic synapsis and sperm formation.
- To explore potential compensatory mechanisms for DNA repair during meiosis.
Main Methods:
- Gene disruption of dmc1 in male medaka.
- Histological examination of medaka testis nuclei.
- Sperm morphology and motility assessment.
- Transcriptome analysis of mutant medaka testes.
Main Results:
- Synapsis was disturbed in dmc1-mutant medaka testes.
- Mutant medaka produced some sperm, albeit with significant malformations (multiple heads/tails).
- A subset of malformed sperm retained motility and insemination ability.
- Transcriptome analysis revealed no major changes in meiotic DNA repair or flagella assembly gene expression.
Conclusions:
- DMC1 disruption in medaka mirrors defects seen in other species, highlighting its conserved role.
- The unexpected sperm production suggests accessory pathways compensate for DMC1 loss in DNA repair.
- Meiotic recombination defects can lead to sperm malformations, impacting male fertility.
- This study provides insights into alternative mechanisms for repairing meiotic double-strand breaks.
