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Creators/Authors contains: "Neylan, Isabelle P."

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  1. Abstract

    Understanding the mechanisms by which individual organisms respond and populations adapt to global climate change is a critical challenge. The role of plasticity and acclimation, within and across generations, may be essential given the pace of change. We investigated plasticity across generations and life stages in response to ocean acidification (OA), which poses a growing threat to both wild populations and the sustainable aquaculture of shellfish. Most studies of OA on shellfish focus on acute effects, and less is known regarding the longer term carryover effects that may manifest within or across generations. We assessed these longer term effects in red abalone (Haliotis rufescens) using a multi‐generational split‐brood experiment. We spawned adults raised in ambient conditions to create offspring that we then exposed to high pCO2(1180 μatm; simulating OA) or low pCO2(450 μatm; control or ambient conditions) during the first 3 months of life. We then allowed these animals to reach maturity in ambient common garden conditions for 4 years before returning the adults into high or low pCO2treatments for 11 months and measuring growth and reproductive potential. Early‐life exposure to OA in the F1 generation decreased adult growth rate even after 5 years especially when abalone were re‐exposed to OA as adults. Adult but not early‐life exposure to OA negatively impacted fecundity. We then exposed the F2 offspring to high or low pCO2treatments for the first 3 months of life in a fully factorial, split‐brood design. We found negative transgenerational effects of parental OA exposure on survival and growth of F2 offspring, in addition to significant direct effects of OA on F2 survival. These results show that the negative impacts of OA can last within and across generations, but that buffering against OA conditions at critical life‐history windows can mitigate these effects.

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  2. Abstract

    Transgenerational plasticity (TGP)—when a parent or previous generation's environmental experience affects offspring phenotype without involving a genetic change—can be an important mechanism allowing for rapid adaptation. However, despite increasing numbers of empirical examples of TGP, there appears to be considerable variation in its strength and direction, yet limited understanding of what causes this variation. We compared patterns of TGP in response to stress across two populations with high versus low historical levels of stress exposure. Specifically, we expected that exposure to acute stress in the population experiencing historically high levels of stress would result in adaptive TGP or alternatively fixed tolerance (no parental effect), whereas the population with low levels of historical exposure would result in negative parental carryover effects. Using a common sessile marine invertebrate,Bugula neritina, and a split brood design, we exposed parents from both populations to copper or control treatments in the laboratory and then had them brood copper‐naïve larvae. We then exposed half of each larval brood to copper and half to control conditions before allowing them to grow to maturity in the field. Maternal copper exposure had a strong negative carryover effect on adult offspring growth and survival in the population without historical exposure, especially when larvae themselves were exposed to copper. We found little to no maternal or offspring treatment effect on adult growth and survival in the population with a history of copper exposure. However, parents from this population produced larger larvae on average and were able to increase the size of their larvae in response to copper exposure, providing a potential mechanism for maintaining fitness and suggesting TGP through maternal provisioning. These results indicate that the ability to adjust offspring phenotype via TGP may be a locally adapted trait and potentially influenced by past patterns of exposure.

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