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Abstract
Breast cancer amplified sequence 2 (BCAS2) is involved in multiple biological processes, including pre-mRNA splicing. However, the physiological roles of BCAS2 are still largely unclear. Here we report that BCAS2 is specifically enriched in spermatogonia of mouse testes. Conditional disruption of Bcas2 in male germ cells impairs spermatogenesis and leads to male mouse infertility. Although the spermatogonia appear grossly normal, spermatocytes in meiosis prophase I and meiosis events (recombination and synapsis) are rarely observed in the BCAS2-depleted testis. In BCAS2 null testis, 245 genes are altered in alternative splicing forms; at least three spermatogenesis-related genes (Dazl, Ehmt2 and Hmga1) can be verified. In addition, disruption of Bcas2 results in a significant decrease of the full-length form and an increase of the short form (lacking exon 8) of DAZL protein. Altogether, our results suggest that BCAS2 regulates alternative splicing in spermatogonia and the transition to meiosis initiation, and male fertility.
Highlights
Breast cancer amplified sequence 2 (BCAS2) is involved in multiple biological processes, including pre-messenger RNAs (mRNA) splicing
We further showed that BCAS2 was involved in pre-mRNA splicing in spermatogonia in the mouse testis
In embryonic day 15.5 (E15.5) and newborn mouse testes, BCAS2 expression was relatively high in the prospermatogonia located in the centre of the seminiferous tubules of the testes
Summary
Breast cancer amplified sequence 2 (BCAS2) is involved in multiple biological processes, including pre-mRNA splicing. Our results suggest that BCAS2 regulates alternative splicing in spermatogonia and the transition to meiosis initiation, and male fertility. Alternative splicing significantly expands the form and function of the genome of organisms with limited gene number and is especially important for highly complex organisms and tissues[4,5]. Rbm[5], a male germ cell splicing factor, is essential for the appropriate alternative splicing of pre-mRNAs involved in spermatid differentiation[17]. We further showed that BCAS2 was involved in pre-mRNA splicing in spermatogonia in the mouse testis. Our data reveal a critical role of BCAS2 involving in pre-mRNA splicing of spermatogonia and the transition to meiosis, and male fertility
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