Barry P Sleckman

(Molecular Cell 69, 879–892.e1–e5; March 1, 2018) During preparation of this article, the images of cells used in the comet assay shown in Figure 5C were inadvertently labeled in the inverted order, and one image was duplicated. These errors do not affect the conclusion of the data, given that the substituted panels were qualitatively equivalent to the correct ones. Moreover, the quantitation of the data, shown in Figure 5D, was not affected. The corrected Figure 5C appears below.

Abstract DNA damage occurs on exposure to genotoxic agents and during physiological DNA transactions. DNA double-strand breaks (DSBs) are particularly dangerous lesions that activate DNA damage response (DDR) kinases, leading to initiation of a canonical DDR (cDDR). This response includes activation of cell cycle checkpoints and engagement of pathways that repair the DNA DSBs to maintain genomic integrity.

In this issue of Neuron,show that a signal transduction pathway normally exploited by the innate immune system in recognizing foreign agents plays a critical role in controlling a synapse’s ability to maintain stability in the efficacy of synaptic transmission over both rapid and prolonged timescales.