果蝇是研究精子发生的理想模式生物,由于其强大的遗传学,精子产生过程中生殖细胞的保守基因和可见形态。我们之前的工作揭示了ocnus(ocn)击倒导致雄性不育,CG9920在ocn敲低后被鉴定为蝇腹部中显著下调的蛋白,提示CG9920在男性生殖中的作用。在这项研究中,我们发现CG9920在蝇睾丸中高表达。蝇睾丸中CG9920敲除导致男性不育,精囊中没有成熟精子。免疫荧光染色显示CG9920的耗竭导致分散的精子细胞核束,没有迁移到睾丸前部区域的伸长锥较少,几乎没有个性化情结。透射电子显微镜显示,CG9920敲低严重破坏了精子发生过程中的线粒体形态发生。值得注意的是,我们发现CG9920可能不直接与Ocn相互作用,而是被STAT92E抑制,它本身间接受到了Ocn的影响。我们提出了一种可能的新的途径,对于黑腹D.melanogaster的精子发生至关重要,由此Ocn间接诱导CG9920表达,可能通过JAK-STAT信号通路抵消其抑制作用。
Drosophila melanogaster is an ideal model organism for investigating spermatogenesis due to its powerful genetics, conserved genes and visible morphology of germ cells during sperm production. Our previous work revealed that ocnus (ocn) knockdown resulted in male sterility, and
CG9920 was identified as a significantly downregulated protein in fly abdomen after ocn knockdown, suggesting a role of
CG9920 in male reproduction. In this study, we found that
CG9920 was highly expressed in fly testes.
CG9920 knockdown in fly testes caused male infertility with no mature sperms in seminal vesicles. Immunofluorescence staining showed that depletion of CG9920 resulted in scattered spermatid nuclear bundles, fewer elongation cones that did not migrate to the anterior region of the testis, and almost no individualization complexes. Transmission electron microscopy revealed that CG9920 knockdown severely disrupted mitochondrial morphogenesis during spermatogenesis. Notably, we found that
CG9920 might not directly interact with Ocn, but rather was inhibited by STAT92E, which itself was indirectly affected by Ocn. We propose a possible novel pathway essential for spermatogenesis in D. melanogaster, whereby Ocn indirectly induces CG9920 expression, potentially counteracting its inhibition by the JAK-STAT signaling pathway.