ArticlePlant, cell & environment2026
CsSPX-PHR/PHL-PHT1 and CsmiR399a-PHO2-PHT1/PHO1 Modules Orchestrate Pi Use Efficiency and Aluminium Tolerance in Tea Plants.
Article in Plant, cell & environment, 2026. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- CsSPX-PHR/PHL-PHT1 and CsmiR399a-PHO2-PHT1/PHO1 Modules Orchestrate Pi Use Efficiency and Aluminium Tolerance in Tea Plants.Plant, cell & environment · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
High aluminium (Al) toxicity in acidic soils limits natural phosphate (Pi) nutrition to Al-hyperaccumulator tea plants, yet how they achieve Pi use efficiency (PUE) and Al tolerance remains elusive. Here, we deciphered Pi signalling networks and regulatory mechanisms underlying tea plant PUE, by functionally characterising Pi signalling components responding to Pi/N status changes and Al/H stress. CsPHT1.4 and CsPHT1.5 are PM-localised transporters expressed in tea root xylem and stem phloem for Pi uptake and redistribution. The physical interactions between CsSPX1a/2 and CsPHR1b/PHL1a under Pi supply repressed CsPHR1b/PHL1a activation of CsPHT1.4 transcription, but CsPHR1b/PHL1a were relieved from inhibition from the interactions for root Pi uptake under Pi deficiency or low Al conditions. Moreover, N-supply activated CsHHO6a suppressed CsSPX1a, and further activated CsPHR1b and CsPHT1.4 for Pi acquisition. High Al/H toxicity up-regulated CsSTOP1a/2a activated CsSPX1a transcription to repress CsPHR1b-CsPHT1.4 and inhibit Pi absorption and root growth. Meanwhile, Pi supply and high Al/H stress activated CsmiR399a to repress CsPHO2 and stabilise CsPHT1.5/CsPHO1 for Pi redistribution in tea plants. CsSPX1a-CsPHR1b-CsPHT1.4 and CsmiR399a-CsPHO2-CsPHT1.5 modules coordinately regulate Pi homoeostasis under Al/H stress and various N- and Pi- nutrition conditions, laying a foundation for genetic improvement of tea PUE and adaptation to stresses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.