ArticlePlant signaling & behavior2012
The bps signal: embryonic arrest from an auxin-independent mechanism in bypass triple mutants.
Article in Plant signaling & behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Genome-wide identification and functional prediction ofMolecular breeding : new strategies in plant improvement · 2023Article
- A cryptic natural variant allele of BYPASS2 suppresses the bypass1 mutant phenotype.Plant physiology · 2023Article
- Recent advances in understanding carotenoid-derived signaling molecules in regulating plant growth and development.Frontiers in plant science · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-distance signaling is essential for coordination of plant development and environmental responses. We originally isolated a tiny mutant named bypass1 (bps1), which has defects in shoot and root development. The bps1 roots overproduce a mobile signal (bps signal) that arrests both root and shoot development. Our recent study demonstrated that all three BPS gene family members prevent ectopic synthesis of the same bps signal.bps multiple mutants show progressively more severe developmental defects. An embryogenesis analysis revealed abnormal cell divisions in all meristem lineages of bps triple mutants. These defects appear to be auxin independent, and arise prior to changes in PLT1 and PLT2 expression.
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Registered trials
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