CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution

Qinchuan Wang (), Erick O. Hernández-Ochoa, Meera C. Viswanathan, Ian D. Blum, Danh C. Do, Jonathan M. Granger, Kevin R. Murphy, An-Chi Wei, Susan Aja, Naili Liu, Corina M. Antonescu, Liliana D. Florea, C. Conover Talbot, David Mohr, Kathryn R. Wagner, Sergi Regot, Richard M. Lovering, Peisong Gao, Mario A. Bianchet, Mark N. Wu, Anthony Cammarato, Martin F. Schneider, Gabriel S. Bever and Mark E. Anderson ()
Additional contact information
Qinchuan Wang: Johns Hopkins School of Medicine
Erick O. Hernández-Ochoa: University of Maryland School of Medicine
Meera C. Viswanathan: Johns Hopkins School of Medicine
Ian D. Blum: Johns Hopkins School of Medicine
Danh C. Do: Johns Hopkins School of Medicine
Jonathan M. Granger: Johns Hopkins School of Medicine
Kevin R. Murphy: Johns Hopkins School of Medicine
An-Chi Wei: National Taiwan University
Susan Aja: Johns Hopkins School of Medicine
Naili Liu: Kennedy Krieger Institute
Corina M. Antonescu: Johns Hopkins Computational Biology Consulting Core
Liliana D. Florea: Johns Hopkins Computational Biology Consulting Core
C. Conover Talbot: Johns Hopkins School of Medicine
David Mohr: Johns Hopkins School of Medicine Genetic Resources Core Facility
Kathryn R. Wagner: Johns Hopkins School of Medicine
Sergi Regot: Johns Hopkins School of Medicine
Richard M. Lovering: University of Maryland School of Medicine
Peisong Gao: Johns Hopkins School of Medicine
Mario A. Bianchet: Johns Hopkins School of Medicine
Mark N. Wu: Johns Hopkins School of Medicine
Anthony Cammarato: Johns Hopkins School of Medicine
Martin F. Schneider: University of Maryland School of Medicine
Gabriel S. Bever: Johns Hopkins School of Medicine
Mark E. Anderson: Johns Hopkins School of Medicine

Nature Communications, 2021, vol. 12, issue 1, 1-17

Abstract: Abstract Antagonistic pleiotropy is a foundational theory that predicts aging-related diseases are the result of evolved genetic traits conferring advantages early in life. Here we examine CaMKII, a pluripotent signaling molecule that contributes to common aging-related diseases, and find that its activation by reactive oxygen species (ROS) was acquired more than half-a-billion years ago along the vertebrate stem lineage. Functional experiments using genetically engineered mice and flies reveal ancestral vertebrates were poised to benefit from the union of ROS and CaMKII, which conferred physiological advantage by allowing ROS to increase intracellular Ca2+ and activate transcriptional programs important for exercise and immunity. Enhanced sensitivity to the adverse effects of ROS in diseases and aging is thus a trade-off for positive traits that facilitated the early and continued evolutionary success of vertebrates.

Date: 2021
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DOI: 10.1038/s41467-021-23549-3

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