Näytä suppeat kuvailutiedot

dc.contributor.authorHukkanen, Mikaela
dc.contributor.authorHsu, Bin‐Yan
dc.contributor.authorCossin‐Sevrin, Nina
dc.contributor.authorCrombecque, Mélanie
dc.contributor.authorDelaunay, Axelle
dc.contributor.authorHollmen, Lotta
dc.contributor.authorKaukonen, Riina
dc.contributor.authorKonki, Mikko
dc.contributor.authorLund, Riikka
dc.contributor.authorMarciau, Coline
dc.contributor.authorStier, Antoine
dc.contributor.authorRuuskanen, Suvi
dc.date.accessioned2023-10-06T10:18:17Z
dc.date.available2023-10-06T10:18:17Z
dc.date.issued2023
dc.identifier.citationHukkanen, M., Hsu, B., Cossin‐Sevrin, N., Crombecque, M., Delaunay, A., Hollmen, L., Kaukonen, R., Konki, M., Lund, R., Marciau, C., Stier, A., & Ruuskanen, S. (2023). From maternal glucocorticoid and thyroid hormones to epigenetic regulation of offspring gene expression : An experimental study in a wild bird species. <i>Evolutionary Applications</i>, <i>16</i>(10), 1753-1769. <a href="https://doi.org/10.1111/eva.13598" target="_blank">https://doi.org/10.1111/eva.13598</a>
dc.identifier.otherCONVID_189063020
dc.identifier.urihttps://jyx.jyu.fi/handle/123456789/89511
dc.description.abstractOffspring phenotype at birth is determined by its genotype and the prenatal environment including exposure to maternal hormones. Variation in both maternal glucocorticoids and thyroid hormones can affect offspring phenotype, but the underlying molecular mechanisms, especially those contributing to long-lasting effects, remain unclear. Epigenetic changes (such as DNA methylation) have been postulated as mediators of long-lasting effects of early-life environment. In this study, we determined the effects of elevated prenatal glucocorticoid and thyroid hormones on handling stress response (breath rate) as well as DNA methylation and gene expression of glucocorticoid receptor (GR) and thyroid hormone receptor (THR) in great tits (Parus major). Eggs were injected before incubation onset with corticosterone (the main avian glucocorticoid) and/or thyroid hormones (thyroxine and triiodothyronine) to simulate variation in maternal hormone deposition. Breath rate during handling and gene expression of GR and THR were evaluated 14 days after hatching. Methylation status of GR and THR genes was analyzed from the longitudinal blood cells sampled 7 and 14 days after hatching, as well as the following autumn. Elevated prenatal corticosterone level significantly increased the breath rate during handling, indicating an enhanced metabolic stress response. Prenatal corticosterone manipulation had CpG-site-specific effects on DNA methylation at the GR putative promoter region, while it did not significantly affect GR gene expression. GR expression was negatively associated with earlier hatching date and chick size. THR methylation or expression did not exhibit any significant relationship with the hormonal treatments or the examined covariates, suggesting that TH signaling may be more robust due to its crucial role in development. This study provides some support to the hypothesis suggesting that maternal corticosterone may influence offspring metabolic stress response via epigenetic alterations, yet their possible adaptive role in optimizing offspring phenotype to the prevailing conditions, context-dependency, and the underlying molecular interplay needs further research.en
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherWiley
dc.relation.ispartofseriesEvolutionary Applications
dc.rightsCC BY 4.0
dc.subject.otherepigenetics
dc.subject.otherhormone
dc.subject.othermaternal effects
dc.subject.othermethylation
dc.subject.otherParus major
dc.subject.otherprenatal
dc.titleFrom maternal glucocorticoid and thyroid hormones to epigenetic regulation of offspring gene expression : An experimental study in a wild bird species
dc.typearticle
dc.identifier.urnURN:NBN:fi:jyu-202310065541
dc.contributor.laitosBio- ja ympäristötieteiden laitosfi
dc.contributor.laitosDepartment of Biological and Environmental Scienceen
dc.type.urihttp://purl.org/eprint/type/JournalArticle
dc.type.coarhttp://purl.org/coar/resource_type/c_2df8fbb1
dc.description.reviewstatuspeerReviewed
dc.format.pagerange1753-1769
dc.relation.issn1752-4571
dc.relation.numberinseries10
dc.relation.volume16
dc.type.versionpublishedVersion
dc.rights.copyright© 2023 the Authors
dc.rights.accesslevelopenAccessfi
dc.subject.ysolinnut
dc.subject.ysoDNA-metylaatio
dc.subject.ysohormonit
dc.subject.ysogeeniekspressio
dc.subject.ysotalitiainen
dc.subject.ysoglukokortikoidit
dc.subject.ysometylaatio
dc.subject.ysofenotyyppi
dc.subject.ysogeenit
dc.subject.ysoepigenetiikka
dc.format.contentfulltext
jyx.subject.urihttp://www.yso.fi/onto/yso/p3363
jyx.subject.urihttp://www.yso.fi/onto/yso/p38350
jyx.subject.urihttp://www.yso.fi/onto/yso/p2589
jyx.subject.urihttp://www.yso.fi/onto/yso/p25831
jyx.subject.urihttp://www.yso.fi/onto/yso/p12931
jyx.subject.urihttp://www.yso.fi/onto/yso/p27978
jyx.subject.urihttp://www.yso.fi/onto/yso/p39205
jyx.subject.urihttp://www.yso.fi/onto/yso/p13074
jyx.subject.urihttp://www.yso.fi/onto/yso/p147
jyx.subject.urihttp://www.yso.fi/onto/yso/p24631
dc.rights.urlhttps://creativecommons.org/licenses/by/4.0/
dc.relation.datasethttps://doi.org/10.6084/m9.figshare.22153001
dc.relation.doi10.1111/eva.13598
jyx.fundinginformationThe study was funded by KLYY foundation (MH), Valto Takala foundation (MH), FIMM-EMBL rotation program (MH), Jenny and Antti Wihuri foundation (MK), Maupertuis Grant (NCS), University of Turku Graduate School (NCS), Ella and Georg Ehrnrooth Foundation (BYH), Turku Collegium for Science and Medicine (AS), European Commission Marie Sklodowska-Curie Fellowship #894963 (AS), and Academy of Finland (#286278 to SR, #332716 to BYH and #325937 to RK).
dc.type.okmA1


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