Identification and characterization of BEND2 as a key regulator of meiosis during mouse spermatogenesis (PRJCA019938)
Here, we report that mouse BEND2 is specifically expressed in spermatogenic cells around meiotic initiation and that it plays an essential role in meiotic progression. Bend2 gene knockout in male mice arrested meiosis at the transition from zygonema to pachynema, disrupted synapsis and DNA double-strand break repair, and induced nonhomologous chromosomal pairing. BEND2 interacted with chromatin-associated proteins that are components of certain transcription-repressor complexes. BEND2-binding sites were identified in diverse chromatin states and enriched in simple sequence repeats. BEND2 inhibited the expression of genes involved in meiotic initiation and regulated chromatin accessibility and the modification of H3K4me3. Therefore, our study identified BEND2 as a previously unknown key regulator of meiosis, gene expression, and chromatin state during mouse spermatogenesis.
Here, we report that mouse BEND2 is specifically expressed in spermatogenic cells around meiotic initiation and that it plays an essential role in meiotic progression. Bend2 gene knockout in male mice arrested meiosis at the transition from zygonema to pachynema, disrupted synapsis and DNA double-strand break repair, and induced nonhomologous chromosomal pairing. BEND2 interacted with chromatin-associated proteins that are components of certain transcription-repressor complexes. BEND2-binding sites were identified in diverse chromatin states and enriched in simple sequence repeats. BEND2 inhibited the expression of genes involved in meiotic initiation and regulated chromatin accessibility and the modification of H3K4me3. Therefore, our study identified BEND2 as a previously unknown key regulator of meiosis, gene expression, and chromatin state during mouse spermatogenesis.