An acclimatory signature from hemolymph and preparative gene expression after lifespan exposure to ocean acidification
Samuel J. Gurr1, Katherine McFarland2,#, Genevieve Bernatchez2, Mark S. Dixon2, Lisa Guy2, Lisa M. Milke2, Matthew E. Poach2, Deborah Hart3, Louis V. Plough4, Dylan H. Redman2, George Sennefelder2, Sheila Stiles2, Gary H. Wikfors2, Dianna K. Padilla5,#, Shannon L. Meseck2,#
Samuel J. Gurr1, Lisa Guy2, Gary Wikfors2, Yuan Liu2, Meghana Parkih2, Genevieve Bernachez2, Shannon L. Meseck2, Katherine McFarland2
1National Research Council Postdoctoral Associate at NOAA, National Marine Fisheries Service, Northeast Fisheries Science Center, 212 Rogers Avenue, Milford, CT 06460, USA
2NOAA, National Marine Fisheries Service, Northeast Fisheries Science Center, 212 Rogers Avenue, Milford, CT 06460, USA
ABSTRACT (drafting)
Resistance to coastal acidification has a basis in cell physiology that is influenced by both “historical” conditions experienced by the population and those in which the individual organism develops. A developmental “mismatch”, sensu Gluckman (2019), is a contrast between the resulting phenotype of an individual and that which otherwise confers optimal responses (fitness) under a different environment post-development. We experimentally produced adult northern bay scallops, Argopecten irradians, with three pCO2 lineages: one with a two generations in moderate pCO2, one with two generations in low pCO2, and a third consisting of low-pCO2 scallops raised for one generation under high acidification. Adults were exposed to matched and mismatched pCO2 to elucidate signatures of habituation from cytological and molecular traits. Inner mitochondrial transmembrane potential (ΔΨm) was greater by OA habituated scallops independent of pCO2 change. Naive hemocytes were reduced yet with increased ΔΨm under novel pCO2 elevation, suggesting OA-induced apoptosis is linked to reduced mitochondrial integrity. Gene expression reaction norms included constitutive and activated transcription my habituated scallops under pCO2 change, and functions included protein repair and mitochondrial uncoupling, respectively.
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