RNA Therapeutics Institute; Program in Bioinformatics and Integrative Biology; Graduate School of Biomedical Sciences
Cell and Developmental Biology | Genetics and Genomics
In male mice, the transcription factor (TF) A-MYB initiates reprogramming of gene expression after spermatogonia enter meiosis. We report that A-MYB activates Tcfl5, a testis-specific TF first produced in pachytene spermatocytes. Subsequently, A-MYB and TCFL5 reciprocally reinforce their own transcription to establish an extensive circuit that regulates meiosis. TCFL5 promotes transcription of genes required for mRNA turnover, pachytene piRNA production, meiotic exit, and spermiogenesis. This transcriptional architecture is conserved in rhesus macaque, suggesting TCFL5 plays a central role in meiosis and spermiogenesis in placental mammals. Tcfl5em1/em1 mutants are sterile, and spermatogenesis arrests at the mid- or late-pachytene stage of meiosis.
Genetics, transcription factors, meiosis, spermiogenesis, spermatogenesis
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DOI of Published Version
bioRxiv 2021.04.04.438419; doi: https://doi.org/10.1101/2021.04.04.438419. Link to preprint on bioRxiv.
Ozata DM, Yu T, Cecchini K, Mou H, Arif A, Colpan C, Biasini A, Gaitendinov I, de Rooij DG, Weng Z, Zamore PD. (2021). The testis-specific transcription factor TCFL5 responds to A-MYB to elaborate the male meiotic program in placental mammals [preprint]. University of Massachusetts Medical School Faculty Publications. https://doi.org/10.1101/2021.04.04.438419. Retrieved from https://escholarship.umassmed.edu/faculty_pubs/2024
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