The effects of prenatal corticosterone and thyroid hormone on great tit (Parus major) DNA methylation and gene expression
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Julkaisu on tekijänoikeussäännösten alainen. Teosta voi lukea ja tulostaa henkilökohtaista käyttöä varten. Käyttö kaupallisiin tarkoituksiin on kielletty.
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Offspring phenotype is determined by genotype and environmental factors such as
maternal hormones during embryonic development. Avian eggs contain multiple
hormones of maternal origin. Differences in egg hormone concentrations are
hypothesized to cause variation in offspring fitness and survival via epigenetic
mechanisms. In this context, my MSc project tested the effects of prenatal
glucocorticoid ‘stress’ and thyroid hormones on offspring DNA methylation and gene
expression of the glucocorticoid receptor (GCR)- and the thyroid hormone receptor
(THR) -genes in a wild avian population. Great tit (Parus major) eggs were injected with
corticosterone (main avian glucocorticoid) and/or thyroid hormones to simulate
variation in maternal hormone deposition. Methylation status and gene expression
were analyzed from longitudinal blood samples taken 7 and 14 days after hatching, as
well as the following autumn. DNA methylation was analyzed by bisulfite conversion
and pyrosequencing, while gene expression was assessed with RT-qPCR. Hormonal
treatment did not significantly impact methylation status at the putative promoter region
of the genes of interest, nor the expression of GCR and THR genes. Although higher
methylation levels are known to inhibit gene expression, GCR promoter methylation
correlated positively with GCR gene expression. This contrasts the canonical view of
the suppressive role of promoter methylation. GCR expression correlated negatively
with reproductive condition and growth. In turn THR did not exhibit any significant
relationship with the examined covariates, leading to the hypothesis that TH signaling
pathways might be more robust due to the crucial role of thyroid hormones in
development.