Syce1, the Synaptonemal complex central element 1, is a key component of the synaptonemal complex (SC) during meiosis [1,3,5,7,8,9]. The SC is crucial for the synapsis of homologous chromosomes, facilitating genetic exchange through crossing-over and accurate homologous chromosome segregation, thus being essential for the production of haploid germ cells and fertility [6,9].

In male mice, Syce1-null mutants lead to non-obstructive azoospermia (NOA) as spermatogenesis is arrested at the pachytene stage [3,5]. In females, Syce1-related mutations or deletions are associated with premature ovarian insufficiency (POI) [1,4,7,8,10]. For instance, in a consanguineous Chinese family, a homozygous deletion in Syce1 in two sisters with POI was found, while their parents had heterozygous deletions [10]. Also, overexpression or knockdown of Syce1 in Sertoli and Leydig cells in mice can activate or suppress steroidogenic genes involved in testosterone and dihydrotestosterone synthesis [2].

In conclusion, Syce1 is vital for meiosis in both male and female germ cells. Studies on Syce1 knockout or mutant models have revealed its critical role in spermatogenesis and oogenesis, with implications for understanding male infertility (such as NOA) and female infertility (such as POI). These models also help in exploring the regulation of steroid hormone synthesis related to reproductive functions.