ArticleScience advances2026
A transcription factor TOE3 simultaneously promotes growth and antiviral immunity by disrupting ABA core module in tobacco.
Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plant immune activation often reduces growth, which is defined as "growth-defense trade-off" (GDT). Uncoupling GDT is promising for breeding of elite cultivars with strong growth and immunity. We previously identified that AP2 transcription factor TARGET OF EARLY3 (TOE3) promotes both growth and antiviral defense. However, the mechanism underlying this GDT uncoupling remains unknown. Here, we find that the amino-terminal domain of TOE3 (T3N) inhibits abscisic acid (ABA) signaling. Mechanistically, T3N binds to an ABA receptor PYL4 to interfere with PYL4-PP2C4 interaction. The PYL4-PP2C4 module regulates tobacco growth and antiviral immunity. Thus, under normal conditions, T3N enhances tobacco growth via down-regulating ABA response. Upon TMV infection, the phosphorylation of T3N is induced. Phosphorylated T3N exhibits stronger binding affinity to PYL4 to further amplify its disruptive effect on PYL4-PP2C4 module and strongly block ABA response, thereby boosting antiviral immunity. These findings reveal how TOE3 uncouples GDT to provide strategies for breeding crops with strong growth and antiviral immunity.
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.