TRANSCRIPTOMIC RESPONSES OF MALE AND FEMALE MEDAKA GONADS TO HYPOXIC STRESS

Hypoxia is a serious global problem affecting marine and freshwater environments worldwide where over 400 “Dead Zones” have been reported by the United Nations to date. Hypoxia is reported to cause severe reproductive impairments in fish causing heavy loss of fishery production over large areas. Laboratory and field studies have demonstrated that hypoxia can affect male and female reproductive systems at various levels. For example, hypoxia can suppress spermatogenesis and decrease sperm motility as well as impair testicular development and sperm production in male fish, and retard gonadal development and oogenesis in female fish. Notwithstanding this, a genome-wide transcriptomic study to investigate the mechanism(s) underlying hypoxia-induced reproductive impairments in fish has not been reported. Here, we report the transcriptome sequencing (RNA-seq) and bioinformatics analysis of ovary and testis tissues of marine medaka (Oryzias melastigma) to determine the differential molecular responses of male and female gonads to hypoxic stress. Functional GO (Gene Ontology), KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway and IPA (Ingenuity Pathway) analyses demonstrated differential gender-specific gene and signaling pathway responses in male and female fish to hypoxic stress. Specifically, our findings revealed the dysregulation of ovarian follicle development, gonad development and steroid metabolic processes through the modulation of activators including leukemia inhibitory factor (LIF), insulin-like growth factor 1 receptor (IGF1R) and follicle stimulating hormone (FSH) in ovary of hypoxic female medaka fish. In contrast, hypoxia caused the deregulation of the steroid hormone biosynthetic pathway and the stimulation of the apoptotic process through TP53 activation in the testis of hypoxic male medaka fish.