Communication between oocytes and granulosa cells is crucial for the development, dormancy, reawakening, and maturation of oocytes. A key player in this interaction is a protein complex known as the exocyst complex. Research conducted using a mouse model has shown that a lack of this complex leads to female infertility.
In numerous mammals, only a finite number of oocytes are tasked with generating the next generation. These oocytes develop within follicles, which are made up of an oocyte and surrounding granulosa cells. Effective communication (crosstalk) between these two cell types is vital for the processes of oocyte formation, dormancy, reawakening, and maturation. Oocytes produce proteins such as c-KIT and GDF9, which are integral to this crosstalk. However, how these proteins are transported within oocytes has been unclear until now.
In this research, scientists discovered that the exocyst complex is critical for the correct transport of c-KIT and GDF9 within oocytes. Experiments with mice lacking the EXOC1 protein, a critical component of the exocyst complex, demonstrated that this absence hampers oocyte reawakening and growth during follicular development and inhibits the proliferation of granulosa cells. Additionally, it was found that c-KIT and GDF9, which should normally be located on the cell membrane or outside the cell, were instead inappropriately stored in the cytoplasm of oocytes lacking EXOC1. Similar patterns were observed in oocytes that were deficient in other exocyst complex components, such as EXOC3 and EXOC7.
These results suggest that the exocyst complex is vital for the appropriate transport of c-KIT and GDF9 within oocytes, and a malfunctioning exocyst complex is associated with female infertility. This research was supported by Scientific Research (B) grants (17H03566, to SM; 19H03142, to SM) and a Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area) (21H00224, to SM) from the Ministry of Education, Culture, Sports, Science, and Technology.
