Meeting Abstract

P2.12  Friday, Jan. 4  Molecular Mechanisms Regulating High Densities of Mitochondria in the Heart Ventricle of Antarctic Icefishes URSCHEL, Matthew/R*; O’BRIEN, Kristin/M; University of Alaska, Fairbanks fsmru@uaf.edu

Antarctic icefishes (family Channichthyidae) do not express the oxygen-binding protein hemoglobin (Hb). Moreover, of the 16 members of this family, six do not express the intracellular oxygen-binding protein myoglobin (Mb) in heart ventricle tissue. Previous work has determined that the loss of Hb and Mb is correlated with a significant increase in mitochondrial density in icefish hearts compared to red-blooded Antarctic fishes. The molecular underpinnings of this difference is unknown, yet recent studies in mammals have suggested that nitric oxide (NO) may be involved. Both Hb and Mb metabolize nitric oxide (NO), and NO stimulates mitochondrial biogenesis. Thus, the absence of Hb and Mb in icefishes may lead to high levels of NO that trigger the mitochondrial biogenic pathway and maintain high densities of mitochondria in cardiac muscle. We measured the expression of key regulatory factors involved in the NO-mediated pathway of mitochondrial biogenesis (PGC-1α, NRF-1), as well as a downstream-target of these factors (citrate synthase (CS)), and the ratio of mitochondrial-to-nuclear DNA (mtDNA:nDNA) in the ventricle tissue of three species of Antarctic fishes that vary in their expression of Hb and Mb: Notothenia coriiceps (+Hb/+Mb), Chionodraco rastrospinosus (-Hb/+Mb) and Chaenocephalus aceratus (-Hb/-Mb). There was no significant difference in the expression of PGC-1α, NRF-1, CS, or mtDNA:nDNA amongst these three species. These results suggest that the high density of mitochondria in icefish heart ventricles may be maintained through a non-canonical pathway of mitochondrial biogenesis that leads to an increase in the surface density of mitochondrial membranes, but not mitochondrial proteins or DNA. This work was supported by NSF grant ANT 04-38778 to K.O.