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- W2513244407 abstract "The C-repeat binding factors (CBFs), also termed dehydration-responsive element-binding protein 1 (DREB1) family members, play crucial roles in the acquisition of stress tolerance, but in trees, the underlying mechanisms of stress tolerance remain elusive. To gain insight into these mechanisms, we isolated five CBF1 orthologs from four poplar sections (Populus spp.) and assessed their expression under drought, cold, heat and salt stress conditions. Globally induced expression in response to cold suggested a correlation between poplar CBF1 expression and the acquisition of cold tolerance. Responses that varied between sections may reflect section-specific stress tolerance mechanisms, suggesting an effect of ecological context on the development of CBF1-mediated stress tolerance in poplar. We then used a genome-wide search strategy in Populus trichocarpa to predict 2263 putative CBF target genes; the identified genes participate in multiple biological processes and pathways. Almost all of the putative target genes contained multiple cis-acting elements that mediate responses to various environmental and endogenous signals, consistent with an important role of CBF1s in an integrated cold regulatory network. Finally, analysis of an association population of 528 individuals of Populus simonii identified six single-nucleotide polymorphisms (false discovery rate Q < 0.10) significantly (P < 0.005) associated with malondialdehyde production and electrolyte leakage, suggesting the potential importance of PsCBF1 in the regulation of some membrane-related functions. Our findings provide new insights into the function of PsCBF1 and shed light on the CBF-mediated regulatory network in poplar." @default.
- W2513244407 created "2016-09-16" @default.
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- W2513244407 date "2016-09-01" @default.
- W2513244407 modified "2023-09-27" @default.
- W2513244407 title "Poplar CBF1 functions specifically in an integrated cold regulatory network" @default.
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- W2513244407 doi "https://doi.org/10.1093/treephys/tpw079" @default.
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