New techniques in genome editing have led to a controversial debate about the opportunities and uncertainties they present for agricultural food production and consumption. In July 2018, the Court of Justice of the European Union defined genome editing as a new process of mutagenesis, which implies that the resulting organisms count as genetically modified and are subject, in principle, to the obligations of EU Directive 2001/18/EG. This paper examines how key protagonists from academia, politics, and the economy strategically framed the debate around genome editing in agriculture in Germany prior to its legal classification by the Court of Justice. It is based on an analysis of 96 official statements, including position papers, press releases, and information brochures. Our study reveals eight strategic frames used in the discourse on genome editing and uncovers the strategies used to disconnect from or connect with the previous discourse on green genetic engineering in the 1970s, 1980s and 1990s. Building on competitive framing theory, the study provides explanations for the use and emergence of counter-framing strategies and their success or failure in the debate around genome editing.

Prolonged ER stress and the associated unfolded protein response (UPR) can trigger programmed cell death. Studies in cancer cell lines demonstrated that the intracellular accumulation of TRAIL receptor-2 (TRAIL-R2) and the subsequent activation of caspase-8 contribute significantly to apoptosis induction upon ER stress. While this might motivate therapeutic strategies that promote cancer cell death through ER stress-induced caspase-8 activation, it could also support the unwanted demise of non-cancer cells. Here, we therefore investigated if TRAIL-R2 dependent signaling towards apoptosis can be induced in pancreatic β cells, whose loss by prolonged ER stress is associated with the onset of diabetes. Interestingly, we found that elevated ER stress in these cells does not result in TRAIL-R2 transcriptional induction or elevated protein levels, and that the barely detectable expression of TRAIL-R2 is insufficient to allow TRAIL-induced apoptosis to proceed. Overall, this indicates that apoptotic cell death upon ER stress most likely proceeds independent of TRAIL-R2 in pancreatic β cells. Our findings therefore point to differences in ER stress response and death decision-making between cancer cells and pancreatic β cells and also have implications for future targeted treatment strategies that need to differentiate between ER stress susceptibility of cancer cells and pancreatic β cells.

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