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A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
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SOHLH2 is essential for synaptonemal complex formation during spermatogenesis in early postnatal mouse testes
Miree Park1, Youngeun Lee1, Hoon Jang1
1Department of Biomedical Science, CHA University, Seongnam-si, Gyeonggi-do 463-400, Republic of Korea.
Scientific Reports
|February 13, 2016
Summary
Spermatogenesis- and oogenesis-specific helix-loop-helix transcription factor 2 (SOHLH2) is crucial for male fertility. This study reveals SOHLH2 regulates synaptonemal complex formation by controlling Sycp1 expression during mouse spermatogonial differentiation.
Area of Science:
- Reproductive Biology
- Molecular Genetics
- Cell Biology
Background:
- Spermatogenesis- and oogenesis-specific helix-loop-helix transcription factor 2 (SOHLH2) is essential for spermatogenesis in mice.
- The precise regulatory mechanisms of SOHLH2 in early spermatogenesis remain unclear.
Purpose of the Study:
- To investigate the role of SOHLH2 in spermatogenesis.
- To elucidate the regulatory mechanisms governing SOHLH2 during early spermatogenesis.
Main Methods:
- Gene expression profiling of Sohlh2-deficient mouse testes.
- Gene ontology analysis.
- Western blot and immunostaining.
- Analysis of synaptonemal complex formation.
- Reporter assays to assess SOHLH2 interaction with the Sycp1 promoter.
Main Results:
- Sohlh2 deficiency altered the abundance of 513 increased and 492 decreased genes in 14-day-old testes.
- Sohlh2 disruption impacted meiotic genes, including Spo11, Dmc1, Msh4, Prdm9, Sycp1, Sycp2, Sycp3, Hormad1, and Hormad2.
- SOHLH2 deficiency led to reduced SYCP3 levels and impaired synaptonemal complex formation during meiosis.
- SOHLH2 directly interacted with the Sycp1 promoter, enhancing its activity.
Conclusions:
- SOHLH2 plays a critical role in spermatogonial differentiation.
- SOHLH2 is essential for the formation of synaptonemal complexes.
- SOHLH2 regulates synaptonemal complex formation through controlling Sycp1 expression.
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