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P58IPK facilitates plant recovery from ER stress by enhancing protein synthesis
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 ...
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Published in: | Plant biotechnology reports 2022-12, Vol.16 (6), p.665-681 |
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Main Authors: | , , , , , , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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
×
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
×
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
×
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. |
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ISSN: | 1863-5466 1863-5474 |
DOI: | 10.1007/s11816-022-00797-3 |