ArticlePlant, cell & environment2025
Overexpression of Tempranillo-Like Proteins Promotes Dormancy Release in Poplar.
Article in Plant, cell & environment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- European ash pangenome reveals widespread structural variation and genetic basis of low ash dieback susceptibility.Nature communications · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Trees in temperate and boreal latitudes synchronize their growth-dormancy cycles with seasonal environmental variations to ensure their survival over the years. Dormancy control is crucial during winter when plants cease growth and establish buds to protect their apical meristems from cold temperatures. To overcome endormancy, initiate bud break, and restore growth, plants must be exposed to a specific duration of chilling, referred to as the chilling requirement, which is species- and ecotype-dependent. In this study, we study the novel roles of two TEMPRANILLO-like genes (TEML1 and TEML2) in the annual cycle of poplar. We demonstrated that Populus TEML genes are regulated by photoperiod, cold temperatures and the circadian clock, and they are induced in buds by short days and chilling treatment. Notably, their function diverges from the role of its Arabidopsis ortholog AtTEM, which regulates FLOWERING LOCUS T (FT) transcription and the photoperiodic flowering transcription. Transcriptomic analysis of apical buds during short days and chilling treatment revealed that the overexpression of TEML1 and TEML2 accelerate dormancy release by modulating the expression of dormancy regulators and growth-promoting genes.
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