Research.
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Coping with challenges
The stress response hypothalamic-pituitary-adrenal (HPA) axis play a central role in how vertebrates integrate environmental change and cope with these changes, influencing survival and reproductive success. Following the perception of a stressor and activation of the HPA axis, a dramatic increase in glucocorticoid hormones mediates shifts in phenotype. Although the HPA axis is highly conserved in vertebrates, regulation of the stress response varies widely within and across populations, resulting in some individuals and populations being better at coping with stressors. I am currently looking in wild tree swallow whether variation in different aspects of the stress response – baseline corticosterone levels, the magnitude of the corticosterone stress response, and the efficacy of negative feedback in this response – influences the ability to survive and reproduce. Using four populations of tree swallows that breed at different latitudes and altitudes and that exhibit different reproductive behavior and life history, we are manipulating the cost of foraging or predation risk to test whether stress responsiveness is linked to behavior, oxidative stress, telomere erosion, gene expression, and fitness within and across populations.
The HPA axis is by nature plastic, so it could be expected that it is HPA flexibility, or plasticity in the plastic regulation of the HPA axis, which connects individual variation in this endocrine process to organismal performance and ultimately fitness. Glucocorticoid concentrations measured over time (i.e., prior to and after stressors) have been mainly used as readouts for HPA flexibility, and they are sometimes linked to health and fitness. Hence, skepticism endures as to what measures sufficiently capture HPA flexibility and thus fitness. I hypothesized that FKBP5 expression, a co-chaperone of the glucocorticoid receptor (GR) complex regulating GR activity and signaling, represents the functional information carried by circulating glucocorticoids that can be interpreted and transduced to the rest of the body via GR and enable HPA flexibility. Additionally, FKBP5 is a primary target for long-term epigenetic programming of HPA axis, altering the functional information content of glucocorticoids depending on the environments experienced by individuals or even their parents. Thus, FKBP5 may be a particularly valuable proxy for HPA flexibility and help understanding how many vertebrates species handle stress within and across generations. I am currently working on determining how FKBP5 relate to HPA flexibility and fitness and whether CpG content in gene regulatory regions could provide genotypes with different latent capacities for DNA methylation and hence phenotypic plasticity.
Early-life stress
Conditions during early-life can shape individual phenotypes in ways that can have long-term consequences on physiology and behavior. Glucocorticoid stress hormones are a major mediator of this developmental programming. Much previous work, focusing primarily on offspring phenotype and performances relatively early in life at a single time point, suggests a potential negative fitness outcome from exposure to stress during early development. However, as the HPA axis plays a central role in coping with environmental pressures, it has been suggested that early-life stress may be adaptive if adult environmental conditions match those experienced during development. I explore the relationship between maternal stress and offspring phenotype from an ecological and evolutionary perspective in order to determine if early-life stress may be adaptive. I aim to better understanding how early-life stress-induced mechanisms may act as translators between environmental variability and phenotypic responses in offspring and the potential adaptive role that early-life stress plays in ecological systems. I am also interested in the mechanisms that may mediate early-life stress effects and transgenerational transmission of these effects, and thus I am especially epigenetics modification that could be induced by early-life conditions and their consequences on genes expression.
The stress response hypothalamic-pituitary-adrenal (HPA) axis play a central role in how vertebrates integrate environmental change and cope with these changes, influencing survival and reproductive success. Following the perception of a stressor and activation of the HPA axis, a dramatic increase in glucocorticoid hormones mediates shifts in phenotype. Although the HPA axis is highly conserved in vertebrates, regulation of the stress response varies widely within and across populations, resulting in some individuals and populations being better at coping with stressors. I am currently looking in wild tree swallow whether variation in different aspects of the stress response – baseline corticosterone levels, the magnitude of the corticosterone stress response, and the efficacy of negative feedback in this response – influences the ability to survive and reproduce. Using four populations of tree swallows that breed at different latitudes and altitudes and that exhibit different reproductive behavior and life history, we are manipulating the cost of foraging or predation risk to test whether stress responsiveness is linked to behavior, oxidative stress, telomere erosion, gene expression, and fitness within and across populations.
The HPA axis is by nature plastic, so it could be expected that it is HPA flexibility, or plasticity in the plastic regulation of the HPA axis, which connects individual variation in this endocrine process to organismal performance and ultimately fitness. Glucocorticoid concentrations measured over time (i.e., prior to and after stressors) have been mainly used as readouts for HPA flexibility, and they are sometimes linked to health and fitness. Hence, skepticism endures as to what measures sufficiently capture HPA flexibility and thus fitness. I hypothesized that FKBP5 expression, a co-chaperone of the glucocorticoid receptor (GR) complex regulating GR activity and signaling, represents the functional information carried by circulating glucocorticoids that can be interpreted and transduced to the rest of the body via GR and enable HPA flexibility. Additionally, FKBP5 is a primary target for long-term epigenetic programming of HPA axis, altering the functional information content of glucocorticoids depending on the environments experienced by individuals or even their parents. Thus, FKBP5 may be a particularly valuable proxy for HPA flexibility and help understanding how many vertebrates species handle stress within and across generations. I am currently working on determining how FKBP5 relate to HPA flexibility and fitness and whether CpG content in gene regulatory regions could provide genotypes with different latent capacities for DNA methylation and hence phenotypic plasticity.
Early-life stress
Conditions during early-life can shape individual phenotypes in ways that can have long-term consequences on physiology and behavior. Glucocorticoid stress hormones are a major mediator of this developmental programming. Much previous work, focusing primarily on offspring phenotype and performances relatively early in life at a single time point, suggests a potential negative fitness outcome from exposure to stress during early development. However, as the HPA axis plays a central role in coping with environmental pressures, it has been suggested that early-life stress may be adaptive if adult environmental conditions match those experienced during development. I explore the relationship between maternal stress and offspring phenotype from an ecological and evolutionary perspective in order to determine if early-life stress may be adaptive. I aim to better understanding how early-life stress-induced mechanisms may act as translators between environmental variability and phenotypic responses in offspring and the potential adaptive role that early-life stress plays in ecological systems. I am also interested in the mechanisms that may mediate early-life stress effects and transgenerational transmission of these effects, and thus I am especially epigenetics modification that could be induced by early-life conditions and their consequences on genes expression.