Die AKM/GFÖM und ihre Förderprojekte seit 1985 mit besonderer Berücksichtigung der von ihr geförderten Tonträger

Die AKM (Gesellschaft der Autoren, Komponisten und Musikverleger) wird meistens nur als (Geld)Einhebungsorganisation verstanden. Sie sorgt jedoch auch dafür, dass die Musikschaffenden zu den Tantiemen für die Nutzung der von Ihnen geschaffenen Werke kommen. Neben diesen Tätigkeiten nimmt sie auch kulturelle Funktionen wahr, indem sie Projekte zur Förderung des österreichischen Musikschaffens finanziell unterstützt und auch selbst solche durchführt. Die vorliegende Arbeit beginnt mit einem geschichtlichen Abriss, der die Entstehung und Weiterentwicklung der AKM nachzeichnet. Darauf folgt eine kurze Einführung in wirtschaftliche und juristische Aspekte, die eine Verwertungsgesellschaft betreffen. Kapitel 4 widmet sich der GFÖM (Gesellschaft zur Förderung österreichischer Musik), einer hundertprozentigen Tochtergesellschaft der AKM. Der Hauptteil der Arbeit beschäftigt sich mit der Darstellung der Förderprojekte der AKM/GFÖM seit 1985. Diese sind: die Tonträgerreihen „Österreichische Musik der Gegenwart“ und „Edition Zeit-Ton“; „Lehrbehelfe für den Schulunterricht“; „Informationspaket Wienerlied“; Sampler „Austrian Sound Odyssey“ und „Projekt pop!“. Der Fokus liegt auf den Tonträgern, die innerhalb dieser Projekte entstanden sind. Abschließend wird ein Vergleich mit einigen nationalen und internationalen Verwertungsgesellschaften, Förderungen betreffend, gezogen.The three letters AKM stand for A= Autoren (lyricists), K= Komponisten (composers) and M= Musikverleger (music publishers). AKM is wideley known as a company, which only collects money. But the authors of musical works and their publishers can easily receive the royalties for public performance and broadcasting of their works from AKM. Beside these activities, AKM looks after cultural functions, by sponsoring musical projects made in Austria. This thesis is concerned with the history of AKM, its subsidiary GFÖM and their own sponsored projects, which are “Österreichische Musik der Gegenwart” and “Edition Zeit-Ton”, “Lehrbehelfe für den Schulunterricht”, “Informationspaket Wienerlied“, Austrian Sound Odyssey” and “Projekt pop!”. Concluding there is drawn an analogy between AKM and national/international collecting societies regarding sponsorship

Efficient hepatitis C virus particle formation requires diacylglycerol acyltransferase-1.

Hepatitis C virus (HCV) infection is closely tied to the lipid metabolism of liver cells. Here we identify the triglyceride-synthesizing enzyme diacylglycerol acyltransferase-1 (DGAT1) as a key host factor for HCV infection. DGAT1 interacts with the viral nucleocapsid core and is required for the trafficking of core to lipid droplets. Inhibition of DGAT1 activity or RNAi-mediated knockdown of DGAT1 severely impairs infectious virion production, implicating DGAT1 as a new target for antiviral therapy

Viral killer toxins induce caspase-mediated apoptosis in yeast

In yeast, apoptotic cell death can be triggered by various factors such as H2O2, cell aging, or acetic acid. Yeast caspase (Yca1p) and cellular reactive oxygen species (ROS) are key regulators of this process. Here, we show that moderate doses of three virally encoded killer toxins (K1, K28, and zygocin) induce an apoptotic yeast cell response, although all three toxins differ significantly in their primary killing mechanisms. In contrast, high toxin concentrations prevent the occurrence of an apoptotic cell response and rather cause necrotic, toxin-specific cell killing. Studies with Δyca1 and Δgsh1 deletion mutants indicate that ROS accumulation as well as the presence of yeast caspase 1 is needed for apoptosis in toxin-treated yeast cells. We conclude that in the natural environment of toxin-secreting killer yeasts, where toxin concentration is usually low, induction of apoptosis might play an important role in efficient toxin-mediated cell killing

Why yeast cells can undergo apoptosis: death in times of peace, love, and war

The purpose of apoptosis in multicellular organisms is obvious: single cells die for the benefit of the whole organism (for example, during tissue development or embryogenesis). Although apoptosis has also been shown in various microorganisms, the reason for this cell death program has remained unexplained. Recently published studies have now described yeast apoptosis during aging, mating, or exposure to killer toxins (Fabrizio, P., L. Battistella, R. Vardavas, C. Gattazzo, L.L. Liou, A. Diaspro, J.W. Dossen, E.B. Gralla, and V.D. Longo. 2004. J. Cell Biol. 166:1055–1067; Herker, E., H. Jungwirth, K.A. Lehmann, C. Maldener, K.U. Frohlich, S. Wissing, S. Buttner, M. Fehr, S. Sigrist, and F. Madeo. 2004. J. Cell Biol. 164:501–507, underscoring the evolutionary benefit of a cell suicide program in yeast and, thus, giving a unicellular organism causes to die for

Changes to lipid droplet configuration in mCMV-infected fibroblasts: live cell imaging with simultaneous CARS and two-photon fluorescence microscopy

We have performed multimodal imaging of live fibroblast cells infected by murine cytomegalovirus (mCMV). The infection process was monitored by imaging the two-photon fluorescence signal from a GFP-expressing strain of mCMV, whilst changes to lipid droplet configuration were observed by CARS imaging. This allowed us to identify three visually distinct stages of infection. Quantitative analysis of lipid droplet number and size distributions were obtained from live cells, which showed significant perturbations across the different stages of infection. The CARS and two-photon images were acquired simultaneously and the experimental design allowed incorporation of an environmental control chamber to maintain cell viability. Photodamage to the live cell population was also assessed

Chronological aging leads to apoptosis in yeast

During the past years, yeast has been successfully established as a model to study mechanisms of apoptotic regulation. However, the beneficial effects of such a cell suicide program for a unicellular organism remained obscure. Here, we demonstrate that chronologically aged yeast cultures die exhibiting typical markers of apoptosis, accumulate oxygen radicals, and show caspase activation. Age-induced cell death is strongly delayed by overexpressing YAP1, a key transcriptional regulator in oxygen stress response. Disruption of apoptosis through deletion of yeast caspase YCA1 initially results in better survival of aged cultures. However, surviving cells lose the ability of regrowth, indicating that predamaged cells accumulate in the absence of apoptotic cell removal. Moreover, wild-type cells outlast yca1 disruptants in direct competition assays during long-term aging. We suggest that apoptosis in yeast confers a selective advantage for this unicellular organism, and demonstrate that old yeast cells release substances into the medium that stimulate survival of the clone

Bidirectional lipid droplet velocities are controlled by differential binding strengths of HCV Core DII protein

Host cell lipid droplets (LD) are essential in the hepatitis C virus (HCV) life cycle and are targeted by the viral capsid core protein. Core-coated LDs accumulate in the perinuclear region and facilitate viral particle assembly, but it is unclear how mobility of these LDs is directed by core. Herein we used two-photon fluorescence, differential interference contrast imaging, and coherent anti-Stokes Raman scattering microscopies, to reveal novel core-mediated changes to LD dynamics. Expression of core protein’s lipid binding domain II (DII-core) induced slower LD speeds, but did not affect directionality of movement on microtubules. Modulating the LD binding strength of DII-core further impacted LD mobility, revealing the temporal effects of LD-bound DII-core. These results for DII-core coated LDs support a model for core-mediated LD localization that involves core slowing down the rate of movement of LDs until localization at the perinuclear region is accomplished where LD movement ceases. The guided localization of LDs by HCV core protein not only is essential to the viral life cycle but also poses an interesting target for the development of antiviral strategies against HCV

An AIF orthologue regulates apoptosis in yeast

Apoptosis-inducing factor (AIF), a key regulator of cell death, is essential for normal mammalian development and participates in pathological apoptosis. The proapoptotic nature of AIF and its mode of action are controversial. Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis. Similar to mammalian AIF, Ynr074cp is located in mitochondria and translocates to the nucleus of yeast cells in response to apoptotic stimuli. Purified Ynr074cp degrades yeast nuclei and plasmid DNA. YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis. Conversely, overexpression of Ynr074cp strongly stimulates apoptotic cell death induced by hydrogen peroxide and this effect is attenuated by disruption of cyclophilin A or the yeast caspase YCA1. We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1)