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Absence of MerTK disrupts spermatogenesis in an age-dependent manner
Jie Shi1, Sheng Gao1, Zhengru Chen1
1Institute of Reproductive Medicine, Medical School of Nantong University, Nantong, 226001, China.
Abstract:
Spermatogenesis is a highly specialized cell differentiation process regulated by the testicular microenvironment. During the process of spermatogenesis, phagocytosis performs an essential role in male germ cell development, and its dysfunction in the testis can cause reproduction defects. MerTK, as a critical protein of phagocytosis, facilitates the removal of apoptotic substrates from the retina and ovaries through cooperation with several phagocytosis receptors. However, its role in mammalian spermatogenesis remains undefined. Here, we found that 30-week-old MerTK-/- male mice developed oligoasthenospermia due to abnormal spermatogenesis. These mice showed damaged seminiferous tubule structure, as well as altered spermatogonia proliferation and differentiation. We also found that Sertoli cells from MerTK-/- mice had decreased phagocytic activity on apoptotic germ cells in vitro. Moreover, a transcriptomic analysis demonstrated that the pivotal genes involved in spermatid differentiation and development changed expression. These results indicate that MerTK is crucial for spermatogenesis, as it regulates the crosstalk between germ cells and Sertoli cells. This provides us insight into the molecular mechanism of MerTK on spermatogenesis and its implications for the diagnosis and treatment of human male infertility.
Insights
The MerTK protein is essential for male fertility, as its absence causes abnormal sperm production and testicular defects in mice. This finding highlights MerTK
Area of Science:
- Reproductive Biology
- Cell Biology
- Molecular Biology
Background:
- Spermatogenesis, the process of sperm production, relies on a specific testicular microenvironment.
- Phagocytosis is crucial for male germ cell development, and its impairment can lead to reproductive issues.
- MerTK (Mer tyrosine kinase) is known to be involved in phagocytosis in other tissues but its role in spermatogenesis is unclear.
Purpose of the Study:
- To investigate the role of MerTK in mammalian spermatogenesis.
- To determine the impact of MerTK deficiency on male reproductive function and testicular structure.
- To elucidate the molecular mechanisms by which MerTK influences spermatogenesis.
Main Methods:
- Generation and analysis of MerTK knockout (MerTK-/-) mice.
- Histological examination of testicular structure and seminiferous tubules.
- In vitro assessment of Sertoli cell phagocytic activity.
- Transcriptomic analysis to identify gene expression changes.
Main Results:
- MerTK-/- male mice exhibited oligoasthenospermia (low sperm count and motility) and abnormal spermatogenesis.
- Histological analysis revealed damaged seminiferous tubules and altered spermatogonia proliferation/differentiation.
- Sertoli cells from MerTK-/- mice showed reduced ability to phagocytose apoptotic germ cells in vitro.
- Transcriptomic data indicated altered expression of key genes involved in spermatid development.
Conclusions:
- MerTK is essential for normal spermatogenesis in mammals.
- MerTK regulates the interaction between germ cells and Sertoli cells, crucial for testicular function.
- Understanding MerTK's role offers potential insights for diagnosing and treating male infertility.
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