ArticlePlant cell reports2025
Cotton GhMAX2 promotes single-celled fiber elongation by releasing the GhS1FA-mediated inhibition of fatty acid biosynthesis.
Article in Plant cell reports, 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
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 function of tea plant CsMORF9.3 in chlorophyll biosynthesis and RNA editing.Plant cell reports · 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
3 authors.
Funding
Abstract
key messageCotton GhMAX2 positively regulates fiber elongation by mediating the degradation of GhS1FA, which transcriptionally represses GhKCS9 expression. Strigolactones (SLs) are known to promote cotton fiber development. However, the precise molecular relationship between SL signaling and fiber cell elongation remains unclear. In this study, we investigate the role of F-box E3 ligase MORE AXILLARY GROWTH2 (MAX2) in upland cotton in relation to the regulation of fiber development. GhMAX2b and GhMAX2f act as key components for SL signal transduction, with their loss-of-function leading to a notable reduction in fiber length. Biochemical analysis showed that GhMAX2b/f trigger the ubiquitination and subsequent degradation of the transcription repressor strigolactone-1-factor-At (GhS1FA), which function as a substrate for these E3 ligases. Furthermore, GhS1FA inhibits fatty acids biosynthesis by directly binding to the W-box element within the promoter of 3-ketoacyl-CoA synthases 9 (GhKCS9) and repressing its expression. In summary, we propose that GhMAX2b/f promote fiber elongation, potentially operating partially independently of GhD53 degradation.
Indexed as
Identifiers
39792241What Socratic 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 Socratic graph.