RBBP7, retinoblastoma binding protein 7, is a core component of many histone modification and chromatin remodeling complexes, regulating chromatin metabolism. It functions in affecting DNA replication, controlling cell proliferation, and is involved in pathways like PI3K/AKT [2,3].

In male reproduction, a hemizygous variant of X-linked RBBP7 was found to cause maturation arrest (MA), a subtype of non-obstructive azoospermia, and was associated with Leydig cell tumors. In mouse spermatogonial and pachytene spermatocyte-derived cells, rbbp7 deprivation led to cell cycle arrest and apoptosis. In Drosophila, knockdown of RBBP7/Caf1-55 in germ cells led to absence of germ cells and reduced testis size, while knockdown in cyst cells caused hyperproliferative testicular cells. Also, male infertility due to Caf1-55 deficiency was rescued by wild-type human RBBP7 [1]. In uterine stromal decidualization in mice, Rbbp7 silencing compromised stromal cell decidualization via attenuating histone H4 acetylation and cyclin D3 expression [4].

In summary, RBBP7 is crucial for spermatogenesis and uterine stromal decidualization. Its mutations or deficiencies can lead to male infertility and testicular tumors, as well as affect uterine development. Research on RBBP7 using genetic models like mouse models has provided insights into these biological processes and associated disease conditions [1,4].