Enterprise Modelling Approach based on Maturity and Business Scope perspectives

This paper introduces a framework that supports users to implement enterprise modelling within collaborative companies. These enterprise models are the basis for a holistic interoperability measurement and management methodology which will be presented in the second part of the paper. The discipline of enterprise modelling aims at capturing all dimensions of an enterprise in a simplified model. Thus enterprise models are the appropriate basis for managing collaborative enterprise as they reduce the complexity of interoperability problems. Therefore, a first objective of this paper is to present an approach that enables companies to get the most effect out of enterprise modelling in a collaborative environment based on the maturity of their organisation relative to modelling. Within this first step, the user will get recommendations e.g. for the correct modelling language as well as the right level of detail.

Organizational excellence through quality governance

This paper provides an overview of an Enterprise Engineering method called IEM (Integrated Enterprise Modeling) and it describes the usage of SIX SIGMA approach for performance measurement of an enterprise. Based on these two instruments a methodology including procedure and tools is developed, which allows enterprises to define their adequate quality criteria for performance, to measure performance and quality and to derive reasonable actions to take for optimization. Determination of adequate quality and performance criteria and reasonable measures for the enterprise organization means “Quality Governance”.

Loss of wobble uridine modification in tRNA anticodons interferes with TOR pathway signaling

Previous work in yeast has suggested that modification of tRNAs, in particular uridine bases in the anticodon wobble position (U34), is linked to TOR (target of rapamycin) signaling. Hence, U34 modification mutants were found to be hypersensitive to TOR inhibition by rapamycin. To study whether this involves inappropriate TOR signaling, we examined interaction between mutations in TOR pathway genes (tip41Δ, sap190Δ, ppm1Δ, rrd1Δ) and U34 modification defects (elp3Δ, kti12Δ, urm1Δ, ncs2Δ) and found the rapamycin hypersensitivity in the latter is epistatic to drug resistance of the former. Epistasis, however, is abolished in tandem with a gln3Δ deletion, which inactivates transcription factor Gln3 required for TOR-sensitive activation of NCR (nitrogen catabolite repression) genes. In line with nuclear import of Gln3 being under control of TOR and dephosphorylation by the Sit4 phosphatase, we identify novel TOR-sensitive sit4 mutations that confer rapamycin resistance and importantly, mislocalise Gln3 when TOR is inhibited. This is similar to gln3Δ cells, which abolish the rapamycin hypersensitivity of U34 modification mutants, and suggests TOR deregulation due to tRNA undermodification operates through Gln3. In line with this, loss of U34 modifications (elp3Δ, urm1Δ) enhances nuclear import of and NCR gene activation (MEP2, GAP1) by Gln3 when TOR activity is low. Strikingly, this stimulatory effect onto Gln3 is suppressed by overexpression of tRNAs that usually carry the U34 modifications. Collectively, our data suggest that proper TOR signaling requires intact tRNA modifications and that loss of U34 modifications impinges on the TORsensitive NCR branch via Gln3 misregulation.

Loss of Anticodon Wobble Uridine Modifications Affects tRNALys Function and Protein Levels in Saccharomyces cerevisiae

In eukaryotes, wobble uridines in the anticodons of tRNALysUUU, tRNAGluUUC and tRNAGlnUUG are modified to 5-methoxy-carbonyl-methyl-2-thio-uridine (mcm5s2U). While mutations in subunits of the Elongator complex (Elp1-Elp6), which disable mcm5 side chain formation, or removal of components of the thiolation pathway (Ncs2/Ncs6, Urm1, Uba4) are individually tolerated, the combination of both modification defects has been reported to have lethal effects on Saccharomyces cerevisiae. Contrary to such absolute requirement of mcm5s2U for viability, we demonstrate here that in the S. cerevisiae S288C-derived background, both pathways can be simultaneously inactivated, resulting in combined loss of tRNA anticodon modifications (mcm5U and s2U) without a lethal effect. However, an elp3 disruption strain displays synthetic sick interaction and synergistic temperature sensitivity when combined with either uba4 or urm1 mutations, suggesting major translational defects in the absence of mcm5s2U modifications. Consistent with this notion, we find cellular protein levels drastically decreased in an elp3uba4 double mutant and show that this effect as well as growth phenotypes can be partially rescued by excess of tRNALysUUU. These results may indicate a global translational or protein homeostasis defect in cells simultaneously lacking mcm5 and s2 wobble uridine modification that could account for growth impairment and mainly originates from tRNALysUUU hypomodification and malfunction.

Verletzlichkeit der Informationsgesellschaft

1986 bis 1988 eintwickelte die Projektjektgruppe verfassungsverträgliche Technikgestaltung (provet) in einer konditionalen Prognose ein Szenario für die Entwicklung und Anwendung der Informationstechnik in Deutschland. Daraus wurden Thesen für die Verletzlichkeit der Gesellschaft und deren Folgen sowie Gestaltungsvorschläge abgeleitet, mit denen die Verletzlichkeit reduziert werden könne. Der Forschungsbericht "Die Verletzlichkeit der Informationsgesellschaft" wurde vor 25 Jahren publiziert. In dem vorliegenden Beitrag prüfen Mitglieder von provet, inwieweit das Szenario und die diesbezügliche angenommene Verletzlichkeit eingetreten sind, ob eine Gegensteuerung gegen zu viel Verletzlichkeit stattfand und welche Rolle die Gestaltungsvorschläge der Studie dabei spielten. Daraus lässt sich mittelbar auch erkennen, wie nützlich der methodische Ansatz der Technikfolgenforschung und die Gestaltungsvorschläge waren und heute sein können.