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   We propose a novel concept of a Systemic Optimal Risk Transfer Equilibrium (SORTE), which is inspired by the Bu ̈hlmann’s classical notion of an Equilibrium Risk Exchange. We provide sufficient general assumptions that guarantee existence, uniqueness, and Pareto optimality of such a SORTE. In both the Bu ̈hlmann and the SORTE definition, each agent is behaving ra- tionally by maximizing his/her expected utility given a budget constraint. The two approaches differ by the budget constraints. In Bu ̈hlmann’s definition the vector that assigns the budget constraint is given a priori. On the contrary, in the SORTE approach, the vector that assigns the budget constraint is endogenously determined by solving a systemic utility maximization. SORTE gives priority to the systemic aspects of the problem, in order to optimize the overall systemic performance, rather than to individual rationality. 

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4. Rapid local and systemic jasmonate signalling drives the initiation and establishment of plant systemic immunity

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   Abstract Successful recognition of pathogen effectors by plant disease resistance proteins, or effector-triggered immunity (ETI), contains the invading pathogen through localized hypersensitive cell death. ETI also activates long-range signalling to establish broad-spectrum systemic acquired resistance (SAR). Here we describe a sensitive luciferase (LUC) reporter that captures the spatial–temporal dynamics of SAR signal generation, propagation and establishment in systemic responding leaves following ETI.JASMONATE-INDUCED SYSTEMIC SIGNAL 1(JISS1) encodes an endoplasmic-reticulum-localized protein of unknown function.JISS1::LUCcaptured very early ETI-elicited SAR signalling, which surprisingly was not affected by classical SAR mutants but was dependent on calcium and was also wound responsive. Both jasmonate biosynthesis and perception mutants abolishedJISS1::LUCsignalling and SAR toPseudomonas syringae. Furthermore, we discovered that ETI initiated jasmonate-dependent systemic surface electrical potentials. These surface potentials were dependent on both glutamate receptors and JISS1, despite neitherJISS1loss-of-function nor glutamate receptor mutants altering SAR toPseudomonas syringae. We thus demonstrate that jasmonate signalling, usually associated with antagonism of defence against biotrophs, is crucial to the rapid initiation and establishment of SAR systemic defence responses (including the activation of systemic surface potentials) and thatJISS1::LUCserves as a reporter to further dissect these pathways. 

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5. On fairness of systemic risk measures

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