ArticleThe New phytologist2026
Auxin-related regulation of barley floral organ fate: genetic and phenotypic insights from tweaky spike mutants.
Article in The New phytologist, 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
11 authors.
Funding
Abstract
Mutant-based research is a cornerstone for elucidating gene function in barley (Hordeum vulgare) and other cereals. In this study, we exploited a unique collection of barley tweaky spike (tw) mutants to identify the locus controlling floret and spike development. We combined genetic mapping with structural variant and gene-expression analyses across a tw allelic series, supported by functional validation, and quantified endogenous auxin levels alongside auxin-application assays to test phytohormone involvement. Analysis of independent tw allelic mutants revealed that the phenotype results from loss of function of HvAP2L5, most often due to complete open reading frame (ORF) deletions, and, in one allele, due to transcriptional silencing. tw mutants showed a reproducible endogenous indole-3-acetic acid deficit, and exogenous auxin could partially phenocopy and/or rescue core tw-associated traits, indicating compromised auxin homeostasis. We conclude that HvAP2L5 is essential for normal spike/floret development and that its loss disrupts auxin balance. Auxin imbalance is a compelling working model that can account for most of the pleiotropic features of tw mutants.
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.