Speedy A governs non-homologous XY chromosome desynapsis as a unique prerequisite for XY loop-axis organization

ABSTRACT: In mouse early pachytene spermatocytes, the X and Y chromosomes undergo rapid non-homologous (NH) synapsis and desynapsis, but the functional significance remains unknown. Here, we report that pachynema-specific knockout of Speedy A (SpdyA) from telomeres caused persistent Y-X NH synapsis, with the entire Y axis synapsed onto the X axis. This persistent Y-X NH synapsis did not interrupt meiotic sex chromosome inactivation, recombination, or sex body formation, but it disrupted X-Y loop-axis organization and homologous X-Y desynapsis, leading to spermatocyte death. Similarly, persistent Y-X NH synapsis was also observed in pachytene spermatocytes lacking TRF1, where SpdyA was frequently lost from X-Y non-pseudoautosomal region (non-PAR) telomeres. Mechanistic studies revealed that the Serin

SUBMITTER: Dongteng Liu 

PROVIDER: S-SCDT-10_1038-S44318-025-00528-8 | biostudies-other |

REPOSITORIES: biostudies-other