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• W2938100222 abstract "In the present study, PeSTZ1, a cysteine-2/histidine-2-type zinc finger transcription factor, was isolated from the desert poplar, Populus euphratica, which serves as a model stress adaptation system for trees. PeSTZ1 was preferentially expressed in the young stems and was significantly up-regulated during chilling and freezing treatments. PeSTZ1 was localized to the nucleus and bound specifically to the PeAPX2 promoter. To examine the potential functions of PeSTZ1, we overexpressed it in poplar 84K hybrids (Populus alba × Populus glandulosa), which are known to be stress-sensitive. Upon exposure to freezing stress, transgenic poplars maintained higher photosynthetic activity and dissipated more excess light energy (in the form of heat) than wild-type poplars. Thus, PeSTZ1 functions as a transcription activator to enhance freezing tolerance without sacrificing growth. Under freezing stress, PeSTZ1 acts upstream of ASCORBATE PEROXIDASE2 (PeAPX2) and directly regulates its expression by binding to its promoter. Activated PeAPX2 promotes cytosolic APX that scavenges reactive oxygen species (ROS) under cold stress. PeSTZ1 may operate in parallel with C-REPEAT-BINDING FACTORS to regulate COLD-REGULATED gene expression. Moreover, PeSTZ1 up-regulation reduces malondialdehyde and ROS accumulation by activating the antioxidant system. Taken together, these results suggested that overexpressing PeSTZ1 in 84K poplar enhances freezing tolerance through the modulation of ROS scavenging via the direct regulation of PeAPX2 expression." @default.
• W2938100222 created "2019-04-25" @default.
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• W2938100222 date "2019-04-23" @default.
• W2938100222 modified "2023-10-14" @default.
• W2938100222 title "Pe <scp>STZ</scp> 1, a C2H2‐type zinc finger transcription factor from <i>Populus euphratica</i> , enhances freezing tolerance through modulation of <scp>ROS</scp> scavenging by directly regulating <i> Pe <scp>APX</scp> 2 </i>" @default.
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• W2938100222 doi "https://doi.org/10.1111/pbi.13130" @default.
• W2938100222 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6790368" @default.
• W2938100222 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30977939" @default.
• W2938100222 hasPublicationYear "2019" @default.
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