Obox1 deficiency induceds subfertility in female mice

Obox1 was considered to be a maternal factor participates in oogenesis and follicle development, but its function remains largely undefined. In this study, we demonstrated that Obox1-null female mice displayed subfertility as evidenced by decreased litter size. Obox1 deficiency resulted in less oocytes production. The levels of female sex hormones and gonadotropins, especially luteinizing hormone (LH), were significantly decreased both in ovaries and serum at diestrus. Further studies showed that Obox1-null ovaries were hypo-reactive to LH. There are still more unruptured follicles in the ovaries after superovulation in Obox1-null ovaries. The number of corpus luteum (CL) and serum concentration of progesterone (P4) reduced, and the steroidogenesis-related genes were aberrant in Obox1-null mice. In conclusion, Obox1 deficiency impaired ovulation and luteinization and led to female subfertility. Wild type (WT) or Obox1 knockout (KO) female mice (6-8 weeks old) were treated with 5 IU PMSG which was followed 46-48 hours later by treatment with 5 IU hCG. Mice were euthanized by cervical dislocation 16 hours after hCG injection and MII oocytes from oviducts were collected for RNA-sequencing.