CaMKII oxidation is a performance/disease trade-off in vertebrate evolution
Erick O. Hernández-Ochoa,
Meera C Viswanathan,
Ian D. Blum,
Jonathan M. Granger,
Kevin R. Murphy,
Corina M. Antonescu,
Liliana D. Florea,
C. Conover Talbot,
Kathryn R Wagner,
Richard M. Lovering,
Mark N. Wu,
Martin F. Schneider,
Gabriel S. Bever,
Mark E. Anderson
Posted 12 Sep 2019
bioRxiv DOI: 10.1101/767525
Posted 12 Sep 2019
Reactive oxygen species (ROS) contribute to health and disease. CaMKII is a widely expressed enzyme whose activation by oxidation of regulatory domain methionines (ox-CaMKII) contributes to cardiovascular disease, asthma, and cancer. Here we integrate comparative genomic and experimental data to show that CaMKII activation by ROS arose more than half-a-billion years ago on the vertebrate stem lineage where it constituted a bridge between ROS and increased intracellular Ca2+ release, exercise responsive gene transcription, and improved performance in skeletal muscle. These enhancements to fight-or-flight physiology were likely key in facilitating a well-evidenced shift in the behavioural ecology of our immediate chordate ancestors, and, in turn, the evolutionary success of vertebrates. Still, the ox-CaMKII innovation for augmenting performance must be considered a critical evolutionary trade-off, as it rendered us more susceptible to common and often fatal diseases linked to excessive ROS.
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