“…Since their formal discovery in the 1890s, mitochondria were for the most part studied by biochemists and physiologists seeking to understand the biochemical and metabolic pathways regulating mitochondrial respiration ( Altmann 1890 ; Green 1959 ; Schneider 1959 ; Ernster and Schatz 1981 ). During this time, mitochondria were viewed as unusual cytological bodies because, unlike any other animal cell componentry, they exhibited an outer double membrane ( Sjostrand 1953 ).…”
Mitochondria are key to energy conversion in virtually all eukaryotes. Intriguingly, despite billions of years of evolution inside the eukaryote, mitochondria have retained their own small set of genes involved in the regulation of oxidative phosphorylation (OXPHOS) and protein translation. Although there was a long-standing assumption that the genetic variation found within the mitochondria would be selectively neutral, research over the past 3 decades has challenged this assumption. This research has provided novel insight into the genetic and evolutionary forces that shape mitochondrial evolution and broader implications for evolutionary ecological processes. Many of the seminal studies in this field, from the inception of the research field to current studies, have been conducted using Drosophila flies, thus establishing the species as a model system for studies in mitochondrial evolutionary biology. In this review, we comprehensively review these studies, from those focusing on genetic processes shaping evolution within the mitochondrial genome, to those examining the evolutionary implications of interactions between genes spanning mitochondrial and nuclear genomes, and to those investigating the dynamics of mitochondrial heteroplasmy. We synthesize the contribution of these studies to shaping our understanding of the evolutionary and ecological implications of mitochondrial genetic variation.
“…Since their formal discovery in the 1890s, mitochondria were for the most part studied by biochemists and physiologists seeking to understand the biochemical and metabolic pathways regulating mitochondrial respiration ( Altmann 1890 ; Green 1959 ; Schneider 1959 ; Ernster and Schatz 1981 ). During this time, mitochondria were viewed as unusual cytological bodies because, unlike any other animal cell componentry, they exhibited an outer double membrane ( Sjostrand 1953 ).…”
Mitochondria are key to energy conversion in virtually all eukaryotes. Intriguingly, despite billions of years of evolution inside the eukaryote, mitochondria have retained their own small set of genes involved in the regulation of oxidative phosphorylation (OXPHOS) and protein translation. Although there was a long-standing assumption that the genetic variation found within the mitochondria would be selectively neutral, research over the past 3 decades has challenged this assumption. This research has provided novel insight into the genetic and evolutionary forces that shape mitochondrial evolution and broader implications for evolutionary ecological processes. Many of the seminal studies in this field, from the inception of the research field to current studies, have been conducted using Drosophila flies, thus establishing the species as a model system for studies in mitochondrial evolutionary biology. In this review, we comprehensively review these studies, from those focusing on genetic processes shaping evolution within the mitochondrial genome, to those examining the evolutionary implications of interactions between genes spanning mitochondrial and nuclear genomes, and to those investigating the dynamics of mitochondrial heteroplasmy. We synthesize the contribution of these studies to shaping our understanding of the evolutionary and ecological implications of mitochondrial genetic variation.
CERTAIN centrally active drugs affect the acetylcholine content of the brain, i.e. cholinesterase inhibitors, morphine, tremorogenic agents (Oxotremorine) and barbiturates which increase the acetylcholine level while cholinolytics (GIARMAN and PEPEU, 1962;HOLMSTEDT, LUNDGREN and SUNDWALL, 1963), insulin coma and hypoxia have the opposite effect (WELSH, 1943; CROSSLAND, ELLIOTT and PAPPIUS, 1955). The drug-induced changes of the acetylcholine level in the brain cannot be explained by a direct action on the enzyme choline acetyltransferase (MORRIS, 1961 ; HOLMSTEDT, LUNDGREN, SCHUBERTH and SUNDWALL, 1965) but may be due to an action on the level of acetyl-CoA which is the acetyl-donor for this enzyme (HEBB, 1962). Consequently, we decided to study the effect of these treatments on the acetyl-CoA in the brain and the results are reported in this paper.
MATERIALS A N D M E T H O D SFemale albino rats weighing 180-220 g were used. They had access to food ad libitum except when the effect of insulin was studied when they were fasted for 24 hr before the experiment. The
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