| Summary: | Cold tolerance is improved by cold stress acclimation (CS-ACC), and the cold tolerance level is ‘remembered’ by plants. However, the underlying signaling mechanisms remain largely unknown. Here, the CS memory mechanism was studied by bioinformation, plant physiological and photosynthetic parameters, and gene expression. We found that CS-ACC induced the acquisition of CS memory and enhanced the maintenance of acquired cold tolerance (MACT) in cucumber seedlings. The H<sub>2</sub>O<sub>2</sub> content and NADPH oxidase activity encoded by <i>CsRBOH</i> was maintained at higher levels during recovery after CS-ACC and inhibition of <i>RBOH</i>-dependent signaling after CS-ACC resulted in a decrease in the H<sub>2</sub>O<sub>2</sub> content, NADPH oxidase activity, and MACT. <i>CsRBOH2</i>, <i>3</i>, <i>4</i>, and <i>5</i> showed high expression during recovery after CS-ACC. Many BZR-binding sites were identified in memory-responsive <i>CsRBOHs</i> promoters, and <i>CsBZR1</i> and <i>3</i> showed high expression during recovery after CS-ACC. Inhibition of <i>RBOH</i>-dependent signaling or brassinosteroids affected the maintenance of the expression of these memory-responsive <i>CsRBOHs</i> and <i>CsBZRs.</i> The photosynthetic efficiency (PE) decreased but then increased with the prolonged recovery after CS-ACC, and was higher than the control at 48 h of recovery; however, inhibition of <i>RBOH</i>-dependent signaling resulted in a lower PE. Further etiolated seedlings experiments showed that a photosynthetic capacity was necessary for CS memory. Therefore, photosynthesis mediated by <i>RBOH</i>-dependent signaling is essential for CS memory.
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