Early developmental carry-over effects on exploratory behaviour and DNA methylation in wild great tits (Parus major)

Adverse, postnatal conditions experienced during development are known to
induce lingering effects on morphology, behaviour, reproduction and
survival. Despite the importance of early developmental stress for shaping
the adult phenotype, it is largely unknown which molecular mechanisms
allow for the induction and maintenance of such phenotypic effects once
the early environmental conditions are released. Here we aimed to
investigate whether lasting early developmental phenotypic changes are
associated with post-developmental DNA methylation changes. We used a
cross-foster and brood size experiment in great tit (Parus major)
nestlings, which induced post-fledging effects on biometric measures and
exploratory behaviour, a validated personality trait. We investigated
whether these post-fledging effects are associated with DNA methylation
levels of CpG sites in erythrocyte DNA. Individuals raised in enlarged
broods caught up on their developmental delay after reaching independence
and became more explorative as days since fledging passed, while the
exploratory scores of individuals that were raised in reduced broods
remained stable. Although we previously found that brood enlargement
hardly affected pre-fledging methylation levels, we found 420 CpG sites
that were differentially methylated between fledged individuals that were
raised in small versus large sized broods. A considerable number of the
affected CpG sites were located in or near genes involved in metabolism,
growth, behaviour and cognition. Since the biological functions of these
genes line up with the observed post-fledging phenotypic effects of brood
size, our results suggest that DNA methylation provides organisms the
opportunity to modulate their condition once the environmental conditions
allow it. In conclusion, this study shows that nutritional stress during
early development associates with indirect, carry-over effects on DNA
methylation. We propose that treatment-associated DNA methylation
differences arise as a consequence of pre-fledging phenotypic changes,
rather than that they cause early environmentally-induced effects.