Accepted_test

Hydrophobic and aerophobic mitochondrial mutational spectrum of birds
by Yury Gusarov | Alina Mikhailova | Bogdan Efimenko | Konstantin Gunbin | Andrey Bushuev | Valentina Burksaya | Konstantin Popadin | Immanuel Kant Baltic Federal University | Immanuel Kant Baltic Federal University | Immanuel Kant Baltic Federal University | Immanuel Kant Baltic Federal University | Lomonosov Moscow State University | University of Antwerp | Immanuel Kant Baltic Federal University
Abstract ID: 304
Event: BGRS-abstracts
Sections: [Sym 5] Section “Population and evolutionary genetics/genomics of wild and domestic animals”

Mitochondria is the main power source of the cell. This organelle contains its own DNA (mtDNA). During replication, it becomes vulnerable to different internal mutagenic factors, like spontaneous deamination or even oxidative damage. The result of it is A to G mutation. In several studies connections between A to G frequency and life-history traits were found. Long-living mammals have more A to G mutations compared to short-living ones. In addition, there is a high difference in mutation rate between cold and warm water fishes. Here we are trying to find such connections for birds. For this research we prepared a unique dataset, containing mtDNA genetic and ecological data for birds. We also used a mutational metric GhAhSkew, which was used in previous studies. In our research we discovered that birds mtDNA mutational rate is much higher compare to mammals. Several life-history traits, which change birds mtDNA mutation frequency, were found: losing ability to fly and gaining ability to dive. These traits had statistically significant PGLS results and high Pagel’s lambda value. On the other hand, the reconstructed mutational spectrum didn't have such results. So we made a reconstruction of ancestral states and found that diving modern birds ancestors had high A to G frequency and non-flying birds ancestors had low one. So we made a hypothesis that modern with mtDNA guanine enrichment are under stabilizing selection to protect remaining adenines.