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The role of promoter cis-element, mRNA capping, and ROS in the repression and salt-inducible expression of AtSOT12 in Arabidopsisopen access

Authors
Chen, J.Wang, B.Chung, J.-S.Chai, H.Liu, C.Ruan, Y.Shi, H.
Issue Date
2015
Publisher
Frontiers Research Foundation
Keywords
AtSOT12; Gene regulation; mRNA capping; Polyadenylation; Promoter analysis; ROS; Salt stress
Citation
Frontiers in Plant Science, v.6, no.NOVEMBER
Indexed
SCIE
SCOPUS
Journal Title
Frontiers in Plant Science
Volume
6
Number
NOVEMBER
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/18493
DOI
10.3389/fpls.2015.00974
ISSN
1664-462X
Abstract
Inducible gene expression is a gene regulatory mechanism central to plant response to environmental cues. The inducible genes are often repressed under normal growth conditions while their expression levels are significantly elevated by conditions such as abiotic stresses. Induction of gene expression requires both cis-acting DNA elements and trans-acting proteins that are modulated through signal transduction pathways. Here we report several molecular events that affect salt induced expression of the Arabidopsis AtSOT12 gene. Promoter deletion analysis revealed that DNA elements residing in the 5′ UTR are required for the salt induced expression of AtSOT12. Cytosine methylation in the promoter was low and salt stress slightly increased the DNA methylation level, suggesting that DNA methylation may not contribute to AtSOT12 gene repression. Co-transcriptional processing of AtSOT12 mRNA including capping and polyadenylation site selection was also affected by salt stress. The percentage of capped mRNA increased by salt treatment, and the polyadenylation sites were significantly different before and after exposure to salt stress. The expression level of AtSOT12 under normal growth conditions was markedly higher in the oxi1 mutant defective of reactive oxygen species (ROS) signaling than in the wild type. Moreover, AtSOT12 transcript level was elevated by treatments with DPI and DMTU, two chemicals preventing ROS accumulation. These results suggest that repression of AtSOT12 expression may require physiological level of ROS and ROS signaling. ? 2015 Chen, Wang, Chung, Chai, Liu, Ruan and Shi.
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