Reactive oxygen species (ROS) play a role in aging and senescence in organisms. The oxidation of methionine (Met) residues in proteins to Met sulfoxide by ROS can cause conformational alteration and functional impairments. Met oxidation is reversed by Met sulfoxide reductase (Msr) A and B. Currently, the repair of oxidized proteins by Msr and Msr-mediated physiological functions are not well understood, especially in higher plants. The down-regulated expression of LcMsrA1/B1 may be involved in the senescence of litchi (Litchi chinensis) fruit. We verified that LcCaM1 is a substrate of LcMsrA1 and LcMsrB1 in vitro and in vivo, and oxidized LcCaM1 could be repaired by LcMsrA1 in combination with LcMsrB1. Moreover, LcMsrA1 and LcMsrB1 play important roles in repairing oxidized Met110 and Met125 residues, respectively, in LcCaM1. Furthermore, the Met oxidation in LcCaM1 did not affect its physical interactions with two LcCaM1-binding senescence-related transcription factors LcNAC13 and LcWRKY1, but enhanced their DNA-binding activities. Therefore, we hypothesized that the down-regulated expression of LcMsrA1/B1 results in the accelerated oxidation of LcCaM1, which enhanced the DNA-binding activities of LcNAC13 and LcWRKY1, thereby activating or repressing the expression of senescence-related genes.
Keywords: Calmodulin; Litchi; Methionine sulfoxide reductase; Reactive oxygen species; Senescence; Transcriptional regulation.
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