Role of the Melanocortin System in Gonadal Steroidogenesis of Zebrafish

17 pages, 2 tables, 5 figures.-- This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license

In teleost, as in other vertebrates, stress affects reproduction. A key component of the stress response is the pituitary secretion of the adrenocorticotropic hormone (ACTH), which binds to the melanocortin 2 receptor (MC2R) in the adrenal glands and activates cortisol biosynthesis. In zebrafish, Mc2r was identified in male and female gonads, while ACTH has been shown to have a physiological role in modulating reproductive activity. In this study, the hypothesis that other melanocortins may also affect how the zebrafish gonadal function is explored, specifically steroid biosynthesis, given the presence of members of the melanocortin signaling system in zebrafish gonads. Using cell culture, expression analysis, and cellular localization of gene expression, our new observations demonstrated that melanocortin receptors, accessory proteins, antagonists, and agonists are expressed in both the ovary and testis of zebrafish (n = 4 each sex). Moreover, melanocortin peptides modulate both basal and gonadotropin-stimulated steroid release from zebrafish gonads (n = 15 for males and n = 50 for females). In situ hybridization in ovaries (n = 3) of zebrafish showed mc1r and mc4r in follicular cells and adjacent to cortical alveoli in the ooplasm of previtellogenic and vitellogenic oocytes. In zebrafish testes (n = 3), mc4r and mc1r were detected exclusively in germ cells, specifically in spermatogonia and spermatocytes. Our results suggest that melanocortins are, directly or indirectly, involved in the endocrine control of vitellogenesis in females, through modulation of estradiol synthesis via autocrine or paracrine actions in zebrafish ovaries. Adult zebrafish testes were sensitive to low doses of ACTH, eliciting testosterone production, which indicates a potential role of this peptide as a paracrine regulator of testicular function.

This research was supported by Spanish State Agency of Research (AEI), grant number AGL2016-74857-C3-3-R and PID2019-103969RB-C33 to JMCR and AGL2017-89648P to JR, Portuguese national funds by FCT-Foundation for Science and Technology through the projects PTDC/CVT-CVT/3205/2020, UIDB/04423/2020 and UIDP/04423/2020 and PTDC/CVT-CVT/3205/2020 to AR and National Agency for Research and Development (ANID), Scholarship Program, DOCTORADO BECAS CHILE fellowship 2013–72140242 to SN

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