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. 2015 Mar 25;16(5):545–546. doi: 10.15252/embr.201540227

Figure 1. Bidirectional control between NMD and the UPR.

Figure 1

(A) In basal conditions, NMD constantly represses the UPR via the degradation of ire1 mRNA and other components of the pathway. Under ER stress, the UPR inhibits NMD via eIF2α phosphorylation, which in turn promotes the accumulation of ire1 mRNA, resulting in a robust UPR activation. (B) NMD determines the threshold for the establishment of a UPR reaction and thus impacts cell fate under ER stress. NMD modulates the amplitude and dynamics of UPR signaling, affecting the termination phase under chronic ER stress.