Key Ingredients for Your Next Semantics Elevator Talk

Abstract. 2012 brought a major change to the semantics research com-munity. Discussions on the use and benefits of semantic technologies are shifting away from the why to the how. Surprisingly this more in stake-holder interest is not accompanied by a more detailed understanding of what semantics research is about. Instead of blaming others for their (wrong) expectations, we need to learn how to emphasize the paradigm shift proposed by semantics research while abstracting from technical details and advocate the added value in a way that relates to the im-mediate needs of individual stakeholders without overselling. This paper highlights some of the major ingredients to prepare your next Semantic

Refining Topological Relations between Regions Considering Their Shapes

peer reviewe

A pathogenic role for histone H3 copper reductase activity in a yeast model of Friedreich's ataxia.

Disruptions to iron-sulfur (Fe-S) clusters, essential cofactors for a broad range of proteins, cause widespread cellular defects resulting in human disease. A source of damage to Fe-S clusters is cuprous (Cu1+) ions. Since histone H3 enzymatically produces Cu1+ for copper-dependent functions, we asked whether this activity could become detrimental to Fe-S clusters. Here, we report that histone H3–mediated Cu1+ toxicity is a major determinant of cellular functional pool of Fe-S clusters. Inadequate Fe-S cluster supply, due to diminished assembly as occurs in Friedreich’s ataxia or defective distribution, causes severe metabolic and growth defects in Saccharomyces cerevisiae. Decreasing Cu1+ abundance, through attenuation of histone cupric reductase activity or depletion of total cellular copper, restored Fe-S cluster–dependent metabolism and growth. Our findings reveal an interplay between chromatin and mitochondria in Fe-S cluster homeostasis and a potential pathogenic role for histone enzyme activity and Cu1+ in diseases with Fe-S cluster dysfunction