Introduction:
TOB1 as a member of the BTG/TOB family and recruits factors such as the CCR4-Not complex to regulate mRNA transcription, translation, and turnover. TOB1 also can interact with CCR4-CAF1 and the cytoplasmic poly (A)-binding protein to stimulate mRNA decay and blocking translation of target gene. Existing literature on the Tob1 gene demonstrates its expression in many adult tissues. Analyses of TOB1 expression in the mouse reproductive tissues indicated TOB1 presence in oocyte and round spermatids and its association with DCP2 suggested that TOB1 is involved with mRNP granules. However, it is still unclear what role TOB1 plays during gametogenesis. In this study to investigate the role of TOB1 in gametogenesis, the effects of genetic deletion of Tob1 on mouse and Drosophila spermatogenesis was studied.
Methods:
Sections of testes from Tob1-/-and Tob1+/+mice were examined by routine histology and immunofluorescence to quantify changes in structure, organization, and markers of spermatogenesis. The expression levels of Tob in male flies was reduced utilizing Tob RNAi. Resulting phenotypes were characterized by immunofluorescence.
Results:
Lack of TOB1 resulted in fragmented acrosomes in the mouse testis implying a role for TOB1 in acrosome biogenesis. Co-localization of TOB1 with PNA-lectin and ACRBP markers confirmed the loss of Tob1 affected acrosomes in round spermatids. Drosophila Tob expression was observed in the individualization complex, that develops from the acrosome precursor in spermatids. Knockdown experiments in Drosophila demonstrated a requirement of Tob in the individualisation of sperm.
Conclusion:
TOB1 is involved in the regulation of acrosome biogenesis in mice, and spermatogenesis in Drosophila. The similarity of the phenotypes in TOB-deficient models of fly and mouse suggest some level of evolutionary conservation for TOB genes in spermatogenesis. The data presented in this study are consistent with TOB1 playing an important role in gametogenesis.