Abstract
Mei-P26, a member of the TRIM-NHL family, plays a pivotal role in Drosophila germline development, including female meiosis. However, its role in male meiosis remains unclear. We observed abnormal spermatid cysts comprising 16 cells in mei-P26 mutant testes, which resulted from spermatid differentiation in the absence of meiosis. The same phenotype was observed in the cysts derived from spermatocytes subjected to mei-P26 knockdown. No cysts undergoing meiosis were observed, and cyclin-dependent kinase 1 (Cdk1) was not activated in the knockdown spermatocytes. However, these phenotypes are unlikely to result from altered phosphorylation of Cdk1, which is necessary for its activation. Instead, aberrant subcellular localization of Cyclin B (CycB) was observed. In wild-type, CycB first migrates into the nucleus of spermatocytes at earlier stages, is then exported from the nucleus, and re-enters the nucleus just before meiosis. By contrast, in mei-P26[mfs1] spermatocytes and mei-P26 knockdown cells, CycB remained accumulated in the nucleus before meiosis. Another M-phase Cyclin, Cyclin A also showed nuclear accumulation in mei-P26 knockdown spermatocytes. Interactions between CycB and the nuclear export factors Emb and Nup62 remained unchanged. Although mammalian PLK1 modifies nuclear export signal of CycB in mitosis, a Drosophila orthologue, Polo, is unlikely to be involved in this meiotic phenotype. The loss of mei-P26 resulted in continuous activation of the meiotic checkpoint, which retains M-phase cyclins within the nucleus until multiple conditions necessary for meiosis are satisfied, thereby preventing Cdk1 from full activation. Our findings will be useful for understanding the role of Mei-P26 in other developmental processes.Key words: meiosis, spermatogenesis, Drosophila, mei-P26, checkpoint, cyclins, Cdk1.
