RpL 38 modulates germ cell differentiation by controlling Bam expression in Drosophila testis

作     者：Yang Fang Fengchao Zhang Fangzhen Zhao Jiajia Wang Xinkai Cheng Fei Ye Jiayu He Long Zhao Ying Su 

作者机构：Key Laboratory of Evolution & Marine Biodiversity (Ministry of Education) and Institute of Evolution & Marine Biodiversity Ocean University of China College of Marine Life Sciences Ocean University of China Fisheries College Ocean University of China 

出 版 物：《Science China Life Sciences》 (中国科学:生命科学(英文版))

年 卷 期：2024年

核心收录：

学科分类：0710[理学-生物学] 07[理学] 071008[理学-发育生物学] 

基　　金：supported by the Laoshan Laboratory (LSKJ202203204) the National Natural Science Foundation of China (32170832, 32170541) the Fundamental Research Funds for Central Universities, China (202012004) 

摘      要：Switching from mitotic spermatogonia to meiotic spermatocytes is critical to producing haploid sperms during male germ cell differentiation. However, the underlying mechanisms of this switch remain largely unexplored. In Drosophila melanogaster, the gene RpL38encodes the ribosomal protein L38, one component of the 60S subunit of ribosomes. We found that its depletion in spermatogonia severely diminished the production of mature sperms and thus led to the infertility of male flies. By examining the germ cell differentiation in testes,we found that RpL38-knockdown blocked the transition from spermatogonia to spermatocytes and accumulated spermatogonia in the testis. To understand the intrinsic reason for this blockage, we conducted proteomic analysis for these spermatogonia populations. Differing from the control spermatogonia, the accumulated spermatogonia in RpL38-knockdown testes already expressed many spermatocyte markers but lacked many meiosis-related proteins, suggesting that spermatogonia need to prepare some important proteins for meiosis to complete their switch into spermatocytes. Mechanistically, we found that the expression of bag of marbles (bam), a crucial determinant in the transition from spermatogonia to spermatocytes, was inhibited at both the mRNA and protein levels upon RpL38 depletion. We also confirmed that the bam loss phenocopied RpL38 RNAi in the testis phenotype and transcriptomic profiling. Strikingly, overexpressing bam was able to fully rescue the testis abnormality and infertility of RpL38-knockdown flies, indicating that bam is the key effector downstream of RpL38 to regulate spermatogonia differentiation. Overall, our data suggested that germ cells start to prepare meiosis-related proteins as early as the spermatogonial stage, and RpL38 in spermatogonia is required to regulate their transition toward spermatocytes in a bamdependent manner, providing new knowledge for our understanding of the transition process from spermatogonia to spe