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.
Highlights
The microrchidia (MORC) protein family forms a conserved class of chromatin remodeling factors found in diverse species from Arabidopsis to human [1]
Morc2b is expressed in germ cells
MORC2B regulates the expression of a number of meiosis-specific genes
Summary
The microrchidia (MORC) protein family forms a conserved class of chromatin remodeling factors found in diverse species from Arabidopsis to human [1]. Human MORC2 recruits histone deacetylases to promoter regions, causing local histone H3 deacetylation and transcriptional repression [3, 4]. MORC2 modulates chromatin relaxation in response to DNA damage [5, 6]. MORC3 binds to H3K4me (trimethylated histone H3 lysine 4) in vitro and localizes to H3K4me3-marked genomic sites [7]. These studies reveal a conserved role for MORC proteins in the regulation of high-order chromatin organization
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