Fig. 2. Stress memory and the molecular pathways to recovery.

(A) A theoretical example of memory formation, where up to thousands of stress-inducible transcripts (blue lines) respond to the initial stress, concurrently with accumulation of signaling molecules and the release of repressive chromatin (red lines). Upon reexposure to a second stress, persistent signaling molecules and a retained accessible conformation of chromatin (solid lines) allow an enhanced stress response. The recovery period is a critical window where plant memory can be consolidated or resetting (dashed lines) can occur. (B) For instance, stress-induced changes in chromatin can be transient (possibly tied to regional accessibility for gene activation) or may persist, acting as a form of stress memory (90). (C) Similarly, signaling molecules may facilitate memory. In addition, signaling molecules can act during the recovery process; for instance, ABA may delay resumption of growth to enable embolism repair (113, 120). (D) KEA3 (potassium antiporter) activity accelerates recovery by relaxing non-photochemical quenching (NPQ) activity after dissipation of excess light stress (121). (E) Epigenetic silencing of FLC relies on the spreading of H3K27me3 specifically during transition to warm (recovery), consolidating repression and memory (66, 123, 124). (F) RNA decay reduces levels of stress-induced transcripts, resulting in resetting; impairment of decay may result in stress memory (161).