Abstract

BackgroundThe neuropeptide Kiss and its receptor KissR are key-actors in the brain control of reproduction in mammals, where they are responsible for the stimulation of the activity of GnRH neurones. Investigation in other vertebrates revealed up to 3 Kiss and 4 KissR paralogs, originating from the two rounds of whole genome duplication in early vertebrates. In contrast, the absence of Kiss and KissR has been suggested in birds, as no homologs of these genes could be found in current genomic databases. This study aims at addressing the question of the existence, from an evolutionary perspective, of the Kisspeptin system in birds. It provides the first large-scale investigation of the Kisspeptin system in the sauropsid lineage, including ophidian, chelonian, crocodilian, and avian lineages.ResultsSauropsid Kiss and KissR genes were predicted from multiple genome and transcriptome databases by TBLASTN. Phylogenetic and syntenic analyses were performed to classify predicted sauropsid Kiss and KissR genes and to re-construct the evolutionary scenarios of both gene families across the sauropsid radiation.Genome search, phylogenetic and synteny analyses, demonstrated the presence of two Kiss genes (Kiss1 and Kiss2 types) and of two KissR genes (KissR1 and KissR4 types) in the sauropsid lineage. These four genes, also present in the mammalian lineage, would have been inherited from their common amniote ancestor. In contrast, synteny analyses supported that the other Kiss and KissR paralogs are missing in sauropsids as in mammals, indicating their absence in the amniote lineage. Among sauropsids, in the avian lineage, we demonstrated the existence of a Kiss2-like gene in three bird genomes. The divergence of these avian Kiss2-like sequences from those of other vertebrates, as well as their absence in the genomes of some other birds, revealed the processes of Kiss2 gene degeneration and loss in the avian lineage.ConclusionThese findings contribute to trace back the evolutionary history of the Kisspeptin system in amniotes and sauropsids, and provide the first molecular evidence of the existence and fate of a Kiss gene in birds.

Highlights

  • The neuropeptide Kiss and its receptor kisspeptin receptors (KissR) are key-actors in the brain control of reproduction in mammals, where they are responsible for the stimulation of the activity of gonadotropin-releasing hormone (GnRH) neurones

  • Prediction of sauropsid Kiss To further assess the Kiss diversity, we investigated the presence of these genes in the genomes from various sauropsid groups: the Indian python as representative of ophidians; the painted turtle and the Chinese turtle as representatives of the chelonians; the American alligator, the saltwater crocodile and the Indian garial as representatives of crocodilians; the chicken, the turkey, the mallard duck, the collared flycatcher, the zebra finch, the medium ground finch, the rock pigeon, the saker falcon, the peregrine falcon, the Tibetan ground-tit, the budgerigar and the Puerto-Rican parrot as representative of birds

  • Considering that the Kiss gene sequences are highly variable among species except for the sequence encoding the Kp(10) and its flanking proteolytic cleavage and alphaamidation site, we focused our predictions on the open reading frame (ORF) containing these sequences

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Summary

Introduction

The neuropeptide Kiss and its receptor KissR are key-actors in the brain control of reproduction in mammals, where they are responsible for the stimulation of the activity of GnRH neurones. All these kisspeptin size-variants encompass the C-terminal 10-amino acid sequence [Kp(10)], which represents the minimal sequence for bioactivity This Kp(10) sequence presents the pecularity to be highly conserved among vertebrates, Both kisspeptin (Kiss) and its receptor (KissR) were demonstrated as crucial players of the reproductive function in mammals [6,7,8,9,10,11]. They act upstream in the gonadotropic axis by activating gonadotropin-releasing hormone (GnRH) neurons and are considered as major puberty gatekeepers and reproduction regulators [12]. Overexpression of kisspeptin can induce precocious puberty onset in human and rodents [14,15,16]

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