Pair disruption in female zebra finches: consequences for offspring phenotype and sensitivity to a social stressor

• Pair disruption affects offspring phenotype in a monogamous and biparental species.
• A change of male partner altered egg quality and delayed maturity in offspring.
• In female offspring, pair disruption boosted growth.
• Pair disruption decreased offspring stress sensitivity.
• These maternal effects do not appear to be mediated by maternal yolk corticosterone.

Maternal effects can result in transgenerational phenotypic plasticity, in which environmental variation experienced by mothers is translated into phenotypic variation in offspring. Although maternal effects have been a focus of much recent research, little is known about the long-term consequences of disturbance of the maternal social environment on offspring phenotype in socially monogamous and biparental species. We hypothesized that pair separation followed by re-pairing may generate maternal effects on offspring development. Here, we gave previously paired female zebra finches access to new males 6 days following removal of their original partner to assess experimentally the effects of re-pairing (an ecologically relevant form of social disturbance) on female reproductive investment, yolk corticosterone concentrations and subsequent offspring phenotype. Pair disruption boosted growth in female offspring and delayed the development of plumage colour sex dimorphism in males. Although yolk corticosterone concentrations were not affected by the treatment, offspring from treated mothers were less responsive to social isolation in a novel environment compared to control offspring. This is, to our knowledge, the first study demonstrating that maternal re-pairing prior to hatching has long-lasting effects on offspring phenotype in a socially monogamous and biparental species. Our results also suggest that prehatching maternal effects of this social disturbance are not mediated by maternal yolk corticosterone. Additional studies are required to determine the potential pathways of these maternal effects (e.g. other hormones, epigenetic programming, protein/nutrient content of eggs, etc.) and their adaptive value.