UMass Chan Medical School Faculty Publications
UMMS Affiliation
RNA Therapeutics Institute; Program in Bioinformatics and Integrative Biology; Graduate School of Biomedical Sciences
Publication Date
2021-04-05
Document Type
Article Preprint
Disciplines
Cell and Developmental Biology | Genetics and Genomics
Abstract
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.
Keywords
Genetics, transcription factors, meiosis, spermiogenesis, spermatogenesis
Rights and Permissions
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
DOI of Published Version
10.1101/2021.04.04.438419
Source
bioRxiv 2021.04.04.438419; doi: https://doi.org/10.1101/2021.04.04.438419. Link to preprint on bioRxiv.
Journal/Book/Conference Title
bioRxiv
Repository Citation
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]. UMass Chan Medical School Faculty Publications. https://doi.org/10.1101/2021.04.04.438419. Retrieved from https://escholarship.umassmed.edu/faculty_pubs/2024
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.
Comments
This article is a preprint. Preprints are preliminary reports of work that have not been certified by peer review.