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Published on: March 3, 2020
MORC2B is essential for meiotic progression and fertility
Baolu Shi1,2, Jiangyang Xue1,2,3, Jian Zhou4
1State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
Abstract:
The microrchidia (MORC) family proteins are chromatin-remodelling factors and function in diverse biological processes such as DNA damage response and transposon silencing. Here, we report that mouse Morc2b encodes a functional germ cell-specific member of the MORC protein family. Morc2b arose specifically in the rodent lineage through retrotransposition of Morc2a during evolution. Inactivation of Morc2b leads to meiotic arrest and sterility in both sexes. Morc2b-deficient spermatocytes and oocytes exhibit failures in chromosomal synapsis, blockades in meiotic recombination, and increased apoptosis. Loss of MORC2B causes mis-regulated expression of meiosis-specific genes. Furthermore, we find that MORC2B interacts with MORC2A, its sequence paralogue. Our results demonstrate that Morc2b, a relatively recent gene, has evolved an essential role in meiosis and fertility.
Insights
The microrchidia (MORC) protein Morc2b is essential for fertility in mice. Its inactivation causes meiotic arrest and sterility by disrupting chromosome synapsis and recombination during germ cell development.
Area of Science:
- Molecular Biology
- Genetics
- Reproductive Biology
Background:
- Microrchidia (MORC) proteins are involved in chromatin remodeling, DNA damage response, and transposon silencing.
- The MORC family has diverse functions across various biological processes.
Purpose of the Study:
- To investigate the function of the mouse Morc2b gene, a rodent-specific member of the MORC family.
- To determine the role of Morc2b in germ cell development and reproductive function.
Main Methods:
- Gene knockout studies in mice to inactivate Morc2b.
- Analysis of spermatocyte and oocyte development, including chromosomal synapsis and meiotic recombination.
- Gene expression analysis of meiosis-specific genes.
Main Results:
- Morc2b arose in the rodent lineage via retrotransposition of Morc2a.
- Inactivation of Morc2b resulted in meiotic arrest and sterility in both male and female mice.
- Morc2b-deficient germ cells showed defects in chromosomal synapsis, impaired meiotic recombination, and increased apoptosis.
- Loss of MORC2B led to dysregulated expression of meiosis-specific genes.
- MORC2B was found to interact with its paralogue MORC2A.
Conclusions:
- Morc2b is a crucial, recently evolved gene essential for successful meiosis and fertility in rodents.
- MORC2B plays a vital role in regulating key meiotic events, including chromosome pairing and recombination.
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