Syncytin-a deficiency compromises murine sperm function by suppressing PRL/PGE2 and PI3K/AKT/mTOR pathway

Syna CKO with inhibitor or activator treatment identified that syna knockout could inhibit the PI3K/AKT/mTOR pathway, Ca²⁺ levels, and elevate caspase 3 expression. Therefore, we propose a hypothesis that syna deficiency exacerbates testicular lipid accumulation and apoptosis by suppressing the PI3K/AKT/mTOR and Ca2+ pathway, ultimately leading to spermatogenic dysfunction and male infertility. The study initially included 3 WT and 3 KO samples.

After quality control and exploratory analysis, one control sample (WT1) was identified as a biological outlier and excluded from the final differential expression analysis.