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microrchidia 2B OKDB#: 5532
 Symbols: Morc2b Species: mouse
 Synonyms: Tce6, 4932411A10Rik  Locus: 17 in Homo sapiens


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General Comment MORC2B is essential for meiotic progression and fertility. Shi B et al. (2018) 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.//////////////////

General function
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Cellular localization
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Ovarian function
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Expression regulated by
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Ovarian localization Oocyte
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Follicle stages
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Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name:
type: null mutation
fertility: infertile - ovarian defect
Comment: MORC2B is essential for meiotic progression and fertility. Shi B et al. (2018) 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.//////////////////

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created: Jan. 25, 2018, 11:48 a.m. by: system   email:
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last update: Jan. 25, 2018, 11:49 a.m. by: hsueh    email:



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