bioRxiv preprint doi: https://doi.org/10.1101/171827; this version posted August 6, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. ketu mutant mice uncover an essential meiotic function for the ancient, putative RNA helicase YTHDC2 Devanshi Jain1, M. Rhyan Puno2,4, Kathryn V. Anderson3, and Scott Keeney1,4 * 1Molecular Biology Program, 2Structural Biology Program, 3Developmental Biology Program, and 4Howard Hughes Medical Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065 USA Running title: Ythdc2 is essential for mouse meiosis Keywords Meiosis, spermatogonia, MEIOC, Bgcn, Bam, RNA binding proteins, gametogenesis *Correspondence: Scott Keeney Howard Hughes Medical Institute Molecular Biology Program Memorial Sloan Kettering Cancer Center 1275 York Ave, Box 97 New York, NY 10065 (212) 639-5182
[email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/171827; this version posted August 6, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. ABSTRACT Mechanisms regulating mammalian meiotic progression are poorly understood. Here we identify mouse YTHDC2 as a critical component of this regulation. A screen yielded a mutant, “ketu”, with male and female sterility caused by a Ythdc2 missense mutation. Mutant germ cells enter meiosis but proceed prematurely to aberrant metaphase and apoptosis.