Fgfr1 signalling in the development of a sexually selected trait in vertebrates, the sword of swordtail fish

Abstract

Background: One of Darwin's chosen examples for his idea of sexual selection through female choice was the "sword", a colourful extension of the caudal fin of male swordtails of the genus Xiphophorus. Platyfish, also members of the genus Xiphophorus, are thought to have arisen from within the swordtails, but have secondarily lost the ability to develop a sword. The sustained increase of testosterone during sexual maturation initiates sword development in male swordtails. Addition of testosterone also induces sword-like fin extensions in some platyfish species, suggesting that the genetic interactions required for sword development may be dormant, rather than lost, within platyfish. Despite considerable interest in the evolution of the sword from a behavioural or evolutionary point of view, little is known about the developmental changes that resulted in the gain and secondary loss of the sword. Up-regulation of msxC had been shown to characterize the development of both swords and the gonopodium, a modified anal fin that serves as an intromittent organ, and prompted investigations of the regulatory mechanisms that control msxC and sword growth.

Ontogenetic stage‐specific quantitative trait loci contribute to divergence in developmental trajectories of sexually dimorphic fins between medaka populations

“…; Iovine ; Offen et al . ), so changes to a single gene involved in fin development can potentially influence all fins. Consistent with this idea, our QTL mapping revealed that some QTL were shared among median fins, although we cannot exclude the possibility that multiple linked genes, instead of a single gene, caused the overlap of QTL.…”

Retinoic Acid Is Involved in the Metamorphosis of the Anal Fin into an Intromittent Organ, the Gonopodium, in the Green Swordtail (Xiphophorus hellerii)

“…Gonopodium development is activated by elevated levels of testosterone in poeciliid fish [8], [12], [13], [61] and we show that elevated levels of testosterone induce further developed gonopodia. Several molecular studies support this view: (1) expression of genes involved in fin ray growth, such as msxC , fgfr1 and shh , is induced by testosterone [9], [19], [20]. It has been suggested that androgen signaling acts upstream of a signaling cascade that results in the activation of downstream effectors, such as Fgf-signaling and msxC , to shape the gonopodium [9], [20], (2) androgen receptors ( ars ) are expressed in the developing gonopodium (this study and [19]) and (3) inhibition of androgen signaling down-regulates gene expression and perturbs gonopodium growth [19].…”

“…shh and its receptor ptc1 are expressed during gonopodium development of G. affinis and inhibition of shh signaling also blocks gonopodium development [19]. Moreover, fgfr1 and msxC are up-regulated in growing gonopodial rays and are thought to promote gonopodium outgrowth [9], [20]. Experiments by Pickford and Atz (1957) suggest a putative role of thyroid signaling.…”

Genetic Basis of a Violation of Dollo’s Law: Re-Evolution of Rotating Sex Combs inDrosophila bipectinata

“…In at least some of these species, small vestigial "swordlets" can be restored by exposure to abnormally high levels of testosterone (Gordon et al 1943). In X. maculatus, a swordless species, a single mutation is sufficient to form a similar (although not identical) fin extension, presumably by enhancing cell response to endogenous testosterone (Offen et al 2008). These observations suggest that the pathway responsible for sword development has decayed only partially following the loss of the sword and can be brought back by changes in a relatively small number of genes.…”