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Gyrfalcons Falco rusticolus adjust CTNS expression to food abundance : a possible contribution to cysteine homeostasis

dc.contributor.authorGalván, Ismael
dc.contributor.authorInácio, Ângela
dc.contributor.authorNielsen, Ólafur K.
dc.date.accessioned2017-08-23T10:38:33Z
dc.date.available2017-08-23T10:38:33Z
dc.date.issued2017
dc.description© Springer-Verlag GmbH Germany 2017pt_PT
dc.description.abstractMelanins form the basis of animal pigmentation. When the sulphurated form of melanin, termed pheomelanin, is synthesized, the sulfhydryl group of cysteine is incorporated to the pigment structure. This may constrain physiological performance because it consumes the most important intracellular antioxidant (i.e., glutathione, GSH), of which cysteine is a constitutive amino acid. However, this may also help avoid excess cysteine, which is toxic. Pheomelanin synthesis is regulated by several genes, some of them exerting this regulation by controlling the transport of cysteine in melanocytes. We investigated the possibility that these genes are epigenetically labile regarding protein intake and thus contribute to cysteine homeostasis. We found in the Icelandic population of gyrfalcon Falco rusticolus, a species that pigments its plumage with pheomelanin, that the expression of a gene regulating the export of cystine out of melanosomes (CTNS) in feather melanocytes of developing nestlings increases with food abundance in the breeding territories where they were reared. The expression of other genes regulating pheomelanin synthesis by different mechanisms of influence on cysteine availability (Slc7a11 and Slc45a2) or by other processes (MC1R and AGRP) was not affected by food abundance. As the gyrfalcon is a strict carnivore and variation in food abundance mainly reflects variation in protein intake, we suggest that epigenetic lability in CTNS has evolved in some species because of its potential benefits contributing to cysteine homeostasis. Potential applications of our results should now be investigated in the context of renal failure and other disorders associated with cystinosis caused by CTNS dysfunction.pt_PT
dc.description.sponsorshipIG is supported by a Ramón y Cajal Fellowship (RYC-2012-10237) and the Project CGL2015-67796-P, both from the Spanish Ministry of Economy and Competitiveness (MINECO).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationOecologia (2017) 184:779–785pt_PT
dc.identifier.doi10.1007/s00442-017-3920-6pt_PT
dc.identifier.issn1432-1939
dc.identifier.urihttp://hdl.handle.net/10451/28742
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relation.publisherversionhttps://link.springer.com/journal/442pt_PT
dc.subjectCTNS pt_PT
dc.subjectCysteine homeostasispt_PT
dc.subjectFood abundancept_PT
dc.subjectGyrfalcon pt_PT
dc.subjectPheomelaninpt_PT
dc.titleGyrfalcons Falco rusticolus adjust CTNS expression to food abundance : a possible contribution to cysteine homeostasispt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage785pt_PT
oaire.citation.issue4pt_PT
oaire.citation.startPage779pt_PT
oaire.citation.titleOecologiapt_PT
oaire.citation.volume184pt_PT
rcaap.rightsrestrictedAccesspt_PT
rcaap.typearticlept_PT

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