LOCALIZATION AND CHANGES OF NUCLEAR PROGESTERONE RECEPTORS IN ZEBRAFISH OOCYTES AND ADJACENT FOLLICULAR CELLS

Abstract

The nuclear progesterone receptor (Pgr) is one of the major mediators for progestin signaling during oocyte ovulation in vertebrates. However, any roles Pgr may play in oocyte growth, and especially in the final oocyte maturation, are controversial. Due to the small size of the oocytes and difficulty in separation of encircled follicular cells from oocytes, little information is available on the location and changes of Pgr in vertebrates. We study the roles of the Pgr in the ovaries of zebrafish, which release eggs daily, by localizing and comparing the changes of Pgr in the oocytes and enclosed follicular layers at all developmental stages and from different times of the day or after treatment with various hormones. The pgr transcript and Pgr protein were expressed in oocytes and follicular cells of early developmental stages (stage I and II). In contrast, Pgr was expressed abundantly in the follicular cells surrounding late developmental stage oocytes (stage IV) but completely absent from stage IV oocytes. Furthermore, the most significant daily changes of pgr transcript were observed in the stage IV follicular cells with the highest level observed at 6 am prior to ovulation and the lowest level at 9 pm. The levels of pgr transcript were upregulated by 17 alpha, 20 beta-dihydroxy-4-pregnen-3-one (DHP) in both stages of I-II and IV oocytes. Intriguingly, estrogen (E2) and human chorionic gonadotropins (hCG) significantly suppressed pgr expression in stage I-II oocytes, while enhancing pgr expression in stage IV oocytes. Presence of Pgr in both oocytes and follicular cells of early stages (stages I-II) suggest roles of Pgr in oocyte growth. Abundant expression and dramatic changes of Pgr in the follicular cells of late stage (stage IV) indicate roles of Pgr during oocyte ovulation. Absence and lack of changes of Pgr in the stage IV ooctyes do not support the role of Pgr in final oocyte maturation.