P58(IPK) facilitates plant recovery from ER stress by enhancing protein synthesis

Abstract

P58(IPK) has been implicated in eukaryotic ER stress responses and viral pathogenesis, however, its biological functions and molecular mechanism in plants are unclear. Prolonged ER stress produced by tunicamycin (TM) increased P58(IPK) mRNA and protein levels in Arabidopsis. Although the growth of 2 x 35S:P58(IPK)-myc plants was less severely inhibited than that of Col-0 plants, TM inhibited the growth of p58(ipk)-2 mutants more severely than that of Col-0 plants. Under prolonged ER stress conditions, the unfolded protein response (UPR)-related genes were expressed at a higher level in the p58(ipk)-2 mutants than in Col-0 plants. Protein synthesis inhibition by TM in 2 x 35S:P58(IPK)-myc plants was lower than in Col-0 plants under prolonged ER stress conditions, however, not significantly different in p58(ipk)-2 mutants. The GST-P58(IPK) protein exhibited both chaperone and RNA-binding activities in a dose-dependent manner. P58(IPK) has been shown to interact with ribosomes, allowing for enhanced protein production on the ER membrane. Following ER stress, 2 x 35S:P58(IPK)-myc plants recovered better than Col-0, but p58(ipk)-2 mutants recovered less than Col-0. These findings reveal that P58(IPK) can promote protein translation in association with ribosomes and contribute to stress recovery in Arabidopsis when induced during the last phase of ER stress.