cbd19deb-5302-4144-8c7c-419708aa200f
Impact food quality on Pace of Life
Life history variation usually aligns along a slow-fast continuum with slow development and low reproductive rate at the slow and opposing traits on the other end. Physiological and behavioural traits are hypothesised to integrate with individual differences in life history into pace-of-life syndromes. Traits generally show covariation that can arise from genetic and environmental influences on phenotypes and constrain the independent evolution of traits, resulting in fitness consequences and impacts on population dynamics. How such syndromes emerge, are maintained and adapt to changes in the environment, is as yet not well described. Here, we manipulated food quality to induce a faster pace-oflife in house mice (Mus musculus) living under semi-natural conditions. Across three generations, we investigated whether this change in life history would induce concurrent changes in risk-taking and stress-coping behaviour. Furthermore, we tested if the observed trait changes could be explained by changes in gene expression profiles. We observed the expected increase in pace-of-life which was mainly explained by faster growth and earlier onset of reproduction. Going along with these changes in life history, we observed a decrease in risk-taking. Furthermore, individuals having a fast pace-of-life and living under high quality food conditions, showed a significant change in katabolic processes of liver gene expression, pointing towards a molecular mechanism involving many metabolic processes. Taken together, our data demonstrate that pace-of-life syndromes can adapt to changes in the environment very fast, relying on inter-and transgenerational plasticity rather than the much slower change in gene frequency due to selective processes alone.
Life history variation usually aligns along a slow-fast continuum with slow development and low reproductive rate at the slow and opposing traits on the other end. Physiological and behavioural traits are hypothesised to integrate with individual differences in life history into pace-of-life syndromes. Traits generally show covariation that can arise from genetic and environmental influences on phenotypes and constrain the independent evolution of traits, resulting in fitness consequences and impacts on population dynamics. How such syndromes emerge, are maintained and adapt to changes in the environment, is as yet not well described. Here, we manipulated food quality to induce a faster pace-oflife in house mice (Mus musculus) living under semi-natural conditions. Across three generations, we investigated whether this change in life history would induce concurrent changes in risk-taking and stress-coping behaviour. Furthermore, we tested if the observed trait changes could be explained by changes in gene expression profiles. We observed the expected increase in pace-of-life which was mainly explained by faster growth and earlier onset of reproduction. Going along with these changes in life history, we observed a decrease in risk-taking. Furthermore, individuals having a fast pace-of-life and living under high quality food conditions, showed a significant change in katabolic processes of liver gene expression, pointing towards a molecular mechanism involving many metabolic processes. Taken together, our data demonstrate that pace-of-life syndromes can adapt to changes in the environment very fast, relying on inter-and transgenerational plasticity rather than the much slower change in gene frequency due to selective processes alone.