Morc2b, a member of the microrchidia (MORC) family, is a germ cell-specific chromatin-remodelling factor. It has an essential role in meiotic progression and fertility, being involved in processes like chromosomal synapsis, meiotic recombination, and regulation of meiosis-specific gene expression [1]. Mouse models are valuable for studying its function.

Inactivation of Morc2b in KO mouse models leads to meiotic arrest and sterility in both male and female mice. Morc2b-deficient spermatocytes and oocytes show failures in chromosomal synapsis, blockades in meiotic recombination, and increased apoptosis. Also, loss of MORC2B causes mis-regulation of meiosis-specific genes. Additionally, MORC2B interacts with its sequence paralogue MORC2A [1]. In sterile mouse hybrids, down-regulated Morc2b is observed, along with failure to compartmentalize gammaH2AX into the pachynema sex (XY) body, defects similar to those in Prdm9-null mutants [2].

In conclusion, Morc2b is crucial for meiosis and fertility as revealed by mouse-based research. The gene knockout mouse models have shown its role in maintaining normal meiotic processes, and its dysregulation may be related to hybrid sterility, providing insights into the mechanisms underlying infertility and speciation [1,2].

References:

1. Shi, Baolu, Xue, Jiangyang, Zhou, Jian, Huang, Xiaoyan, Wang, P Jeremy. 2018. MORC2B is essential for meiotic progression and fertility. In PLoS genetics, 14, e1007175. doi:10.1371/journal.pgen.1007175. https://pubmed.ncbi.nlm.nih.gov/29329290/

2. Mihola, Ondrej, Trachtulec, Zdenek, Vlcek, Cestmir, Schimenti, John C, Forejt, Jiri. 2008. A mouse speciation gene encodes a meiotic histone H3 methyltransferase. In Science (New York, N.Y.), 323, 373-5. doi:10.1126/science.1163601. https://pubmed.ncbi.nlm.nih.gov/19074312/