Abstract
The neuropeptides gonadotropin-releasing hormone (GnRH) and kisspeptin (KiSS), and their receptors gonadotropin-releasing hormone receptor (GnRHR) and kisspeptin receptor (KiSSR) play key roles in vertebrate reproduction. Multiple paralogous isoforms of these genes have been identified in various vertebrate species. Two rounds of genome duplication in early vertebrates likely contributed to the generation of these paralogous genes. Genome synteny and phylogenetic analyses in a variety of vertebrate species have provided insights into the evolutionary origin of and relationship between paralogous genes. The paralogous forms of these neuropeptides and their receptors have coevolved to retain high selectivity of the ligand–receptor interaction. These paralogous forms have become subfunctionalized, neofunctionalized, or dysfunctionalized during evolution. This article reviews the evolutionary mechanism of GnRH/GnRHR and KiSS/KiSSR, and the fate of the duplicated paralogs in vertebrates.
Highlights
Neuropeptides serve as messenger molecules to regulate a variety of physiological functions in the nervous and neuroendocrine systems of vertebrates (Hoyle, 1999)
The function of gonadotropin-releasing hormone (GnRH) and gonadotropin-releasing hormone receptor (GnRHR) is critical for sexual maturation and reproduction
The existence of GnRH- and GnRHRlike molecules in early vertebrates and invertebrates tells us that regulation of reproduction is highly conserved in animal phyla (Tello and Sherwood, 2009; Lindemans et al, 2011)
Summary
Neuropeptides serve as messenger molecules to regulate a variety of physiological functions in the nervous and neuroendocrine systems of vertebrates (Hoyle, 1999). The GnRH/kisspeptin system has been well characterized in rodents, which only have one KiSS1 and one GnRH1 ligand–receptor pair, the function of the paralogous genes in other vertebrates remains poorly understood. Some non-mammalian vertebrate species do not have orthologous genes for KiSS1/KiSS1R or GnRH1/GnRHRm1, suggesting that a paralogous set of the genes may substitute for the function of the absent genes.
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