A Critical Role for Oxidative Regulation of CaMKII in the Origin of Vertebrates


Meeting Abstract

P3-155  Sunday, Jan. 6 15:30 – 17:30  A Critical Role for Oxidative Regulation of CaMKII in the Origin of Vertebrates WANG, Q*; HERNANDEZ-OCHOA, E; BLUM, I; VISWANATHAN, M; GRANGER, J; YANG, J; LOVERING, R; SCHNEIDER, M; CAMMARATO, A; WU, M; BEVER, G; ANDERSON, M; Johns Hopkins Univ., School of Medicine; Univ. of Maryland, School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine; Univ. of Maryland, School of Medicine; Univ. of Maryland, School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine; Johns Hopkins Univ., School of Medicine qinchuan.wang@jhmi.edu

Origins pose difficult problems for evolutionary biologists. Comparative analyses are powerful at identifying the stem lineage along which a particular feature finds its origin but relatively weak at providing details of the origin itself. Fossils can mitigate this weakness, and experimental biology is becoming increasingly adept at engineering meaningful outgroups and ancestral conditions. We explore the integration of these approaches for our understanding of vertebrate origins; in particular the emergence along the vertebrate stem lineage of a metabolically active, predatory existence from the sessile, filter-feeding ecology of our deuterostome ancestors. We identify oxidative-mediated activity of the Calcium/Calmodulin-Dependent Protein Kinase II (CaMKII) as a key innovation that helped facilitate the functional potential of such iconic vertebrate apomorphies as an internal skeleton, sympathetic nervous system, increasingly efficient respiratory and circulatory systems, prechordal head, and placode-derived organs of special sensation. Using mutant taxonomic strains that lie phylogenetically inside and outside crown-clade Vertebrata, we provide support that the acquisition of this oxidative-mediated kinase activity ushered in a number of novel modalities for stem vertebrates that included heightened performance of skeletal muscle. The cruel irony of these results is that the same oxidative regulatory pathway that likely played a key role in our early success as vertebrates is also identified in a number of human disease processes, including heart disease, pulmonary disease, and cancer.

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