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Steroid Sensitive <i>kiss2</i> Neurones in the Goldfish: Evolutionary Insights into the Duplicate Kisspeptin Gene‐Expressing Neurones
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Description
<jats:p>The <jats:italic>KISS1/Kiss1/kiss1</jats:italic> gene product kisspeptin is suggested to be involved in the steroid feedback system in vertebrates. In addition to <jats:italic>kiss1</jats:italic>, <jats:italic>kiss2</jats:italic> has been identified in many vertebrates, including some mammals, suggesting that the both genes were originally expressed in the common ancestor of teleosts and tetrapods. Moreover, peptides from both genes have been shown to activate the kisspeptin receptors. To investigate the involvement of <jats:italic>kiss1</jats:italic> or <jats:italic>kiss2</jats:italic> neurones in steroid feedback, we used a seasonal breeder, the goldfish (<jats:italic>Carassius auratus</jats:italic>). We found that <jats:italic>kiss2</jats:italic> is expressed in the preoptic area (POA), nucleus lateralis tuberis and nucleus recessus lateralis, and that <jats:italic>kiss1</jats:italic> is expressed in the habenula. Greater mRNA expression in breeding than in nonbreeding condition animals and conspicuous up‐regulation of gene expression by gonadal steroids was seen only in the <jats:italic>kiss2</jats:italic> neurones of the POA. Furthermore, double <jats:italic>in situ</jats:italic> hybridisation suggested that these neurones express oestrogen receptors. Given that amphibians express <jats:italic>kiss2</jats:italic> in POA and mammalian anteroventral periventricular nucleus/POA <jats:italic>Kiss1</jats:italic> neurones show similar expression dynamics as goldfish POA <jats:italic>Kiss2</jats:italic> neurones, we hypothesise that <jats:italic>kiss1</jats:italic> and <jats:italic>kiss2</jats:italic> share the same evolutionary origin; and, after the loss of <jats:italic>kiss2</jats:italic>, <jats:italic>kiss1</jats:italic> became active for steroid feedback in mammals.</jats:p>
Journal
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- Journal of Neuroendocrinology
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Journal of Neuroendocrinology 24 (6), 897-906, 2012-05-10
Wiley
