Untersuchungen zur Mutation plasmatischer Erbträger,besonders der Plastiden

Ohne ZusammenfassungMit 2 TextabbildungenHerrn Prof. Dr. Dr. h. c.O. Renner zum 75. Geburtstag gewidmet.     

Modellversuche zur Plastiden- und Plasmavererbung

Zusammenfassung Es werden Modellversuche beschrieben, die, auf der Grundlage der Zahl der Plasmabestandteile je Zelle aufbauend, eine Unterscheidung zwischen einer Plastiden-, Chondriosomen-, Sphaerosomen (Mikrosomen)-und Zytoplasmavererbung erlauben. Es wird gezeigt, daß bei Chlorophyllschecken, bei denen Mischzellen mit verschiedenen Plastidentypen prinzipiell fehlen, keine Plastidenvererbung vorliegen kann, auch wenn eine mütterliche, nichtmendelnde Vererbung erfolgt. In einigen solchen Fällen konnte wahrscheinlich gemacht werden, daß die Erbunterschiede in den Chondriosomen oder noch wahrscheinlicher in den Sphaerosomen lokalisiert sind.Mit 4 TextabbildungenHerrn Prof.H. Kappert zum 65. Geburtstag gewidmet     

The size of mitochondrial DNA from a cytoplasmic petite mutant of Saccharomyces cerevisiae

Summary Mitochondrial DNA has been isolated from a cytoplasmic petite mutant of Saccharomyces cerevisiae which has retained only about 2% of the mitochondrial wild type genome. The denatured DNA was analyzed by agarose gel electrophoresis and a homogeneous, single band of DNA was found. Petite and wild type mitochondrial DNAs exhibited similar gel electrophoretic mobilities. Using denatured DNA from the E. coli phages T4 and T3 for comparison a molecular weight of 55×10⁶ daltons has been calculated for the double-stranded petite mitochondrial DNA. On the basis of this observation most of the mitochondrial DNA of this petite mutant appeared to consist of a polymer of about 50 repeats to account for a size similar to that of the wild type molecule. Thus a regulatory mechanism might exist which keeps constant the physical size of the mitochondrial DNA molecule in spite of the elimination of large fractions of the wild type genome.Dedicated to Dr. Dr. h. c. Peter Michaelis on the occasion of his 75th birthday     

Inhibition of histone acetylation and deacetylation enzymes affects longevity,development, and fecundity in the pea aphid (Acyrthosiphon pisum)

Histone acetylation is an evolutionarily conserved epigenetic mechanism of eukaryotic gene regulation which is tightly controlled by the opposing activities of histone acetyltransferases (HATs) and histone deacetylases (HDACs). In insects, life-history traits such as longevity and fecundity are severely affected by the suppression of HAT/HDAC activity, which can be achieved by RNA-mediated gene silencing or the application of chemical inhibitors. We used both experimental approaches to investigate the effect of HAT/HDAC inhibition in the pea aphid (Acyrthosiphon pisum) a model insect often used to study complex life-history traits. The silencing of HAT genes (kat6b, kat7, and kat14) promoted survival or increased the number of offspring, whereas targeting rpd3 (HDAC) reduced the number of viviparous offspring but increased the number of premature nymphs, suggesting a role in embryogenesis and eclosion. Specific chemical inhibitors of HATs/HDACs showed a remarkably severe impact on life-history traits, reducing survival, delaying development, and limiting the number of offspring. The selective inhibition of HATs and HDACs also had opposing effects on aphid body weight. The suppression of HAT/HDAC activity in aphids by RNA interference or chemical inhibition revealed similarities and differences compared to the reported role of these enzymes in other insects. Our data suggest that gene expression in A. pisum is regulated by multiple HATs/HDACs, as indicated by the fitness costs triggered by inhibitors that suppress several of these enzymes simultaneously. Targeting multiple HATs or HDACs with combined effects on gene regulation could, therefore, be a promising approach to discover novel targets for the management of aphid pests.