ArticleNature plants2026
A STRUBBELIG-NHL3 cell surface receptor complex mediates the response to cellulose deficiency in Arabidopsis.
Article in Nature plants, 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.
- The Plant Cell Wall: From Structural Diversity and Biosynthesis to Integrity Signaling and Physiological Functions.Plants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Plant cells are enclosed by a semi-rigid cell wall with a complex biochemical composition and architecture. The poorly understood process of remodelling the cell wall is crucial for controlling growth and development and for regulating abiotic and biotic stress responses. Cell wall remodelling upon disruption of cell wall integrity through inhibition of cellulose biosynthesis depends on the receptor kinase STRUBBELIG (SUB) and its binding partner QUIRKY (QKY). Here, we identify NON-RACE SPECIFIC DISEASE RESISTANCE/HIN1 HAIRPIN-INDUCED-LIKE protein 3 (NHL3) as an additional factor involved in the SUB-dependent cellulose biosynthesis inhibition response. Collectively, our data indicate that NHL3 maintains SUB at the plasma membrane by physically interacting with SUB. SUB signalling is attenuated by receptor-mediated endocytosis initiated by release of first the SUB-NHL3 and later the SUB-QKY interaction. Our results further suggest a diverse set of biochemically and functionally distinct SUB complexes involved in regulating cell wall integrity and development.
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Registered trials
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