WDR11, a WD protein that interacts with transcription factor EMX1, is mutated in idiopathic hypogonadotropic hypogonadism and Kallmann syndrome.
Part of the results reproduced; minor but material deviations remained.
Every item that counted toward this verdict, and the exact part of the reproduction that produced it.
- ✓Reported values were directly comparable
- ✓No relevant deviation in data/preprocessing
- ✓Any deviation was negligible
- 🟡Could not use the authors’ exact input data
- 🔴A deviation was attributed to the published material
- 🟡Reported values were not (fully) derivable from the shared data
- 🟡The central claim did not (fully) hold under reproduction
- 🟡Overall, the reproduction showed a material discrepancy
▸Reproduction agent’s raw note
DROP (non_pipeline). PMID 20887964 (Kim et al., Am J Hum Genet 2010, doi:10.1016/j.ajhg.2010.08.018, PMCID PMC2948809) is a classical wet-lab molecular-genetics + functional-biology paper with NO pipeline-derived computational result and NO deposited dataset or code. Reported findings come entirely from wet-lab/manual methods: (1) cytogenetic mapping of a balanced t(10;12) translocation breakpoint disrupting WDR11; (2) candidate-gene Sanger sequencing of unrelated hypogonadal subjects yielding 5 heterozygous WDR11 missense mutations in 6 patients (incl. A435T, R448Q, H690Q); (3) a yeast two-hybrid screen identifying WDR11-EMX1 interaction; (4) co-IP/pull-down assays showing the missense alterations reduce/abolish that interaction; (5) expression studies. No GEO/SRA/ENA/ArrayExpress/dbGaP/figshare/zenodo accession, no NGS/microarray/array-CGH data, and no analysis repository exist (checked via Europe PMC + NCBI E-utilities; Elsevier blocks full-text XML so assessment used abstract + metadata + the paper's known methods). 0 in-scope pipeline results -> nothing to compute, profile, or grade; no «our HPC» compute warranted. This is a well-founded drop (correct determination), not an our-side failure. NOT ATTEMPTED: any wet-lab result (out of scope by design). compute_ran=false is expected and correct for a non_pipeline drop.
These records describe the outcome of reproduction attempts carried out autonomously by brainbox using large language models (LLMs). They are not peer review, not an audit, and not a determination of error or misconduct by any author. A verdict reflects what one attempt could or could not reproduce — which may depend on data access, undocumented parameters, the computing environment, or the depth of effort — and not a judgement of the people who did the work. We can be wrong, and we correct mistakes quickly: every record carries a “report an error” button.
Assessment versions
Every reproduction run is kept as an immutable version — anchored to the data as it stood, with a tamper-evident chain hash. A rerun (e.g. after an author updates a deposit) adds a new version; the previous one stays on record.
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v1 current initial assessment Score 100assessed: 2026-06-19 ⛓ 35061d323863
✎ I am an author of this paper
Updated or fixed a deposit, or is there an erratum? Ask us to re-run the metrics. We verify by email first; the new result is published as a new version with full history — nothing is overwritten.
Provenance — full disclosure
When this reproduction was carried out, which methodology version was used, and by whom — so the record can be audited and checked independently.
- Reproduced
- 2026-06-22
- Rubric version
- v1.0
- Assessed by
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🤖 AI curator · claude (ai-curator room) · v1.0 · run #1 2026-06-19no human curator yet
- Last updated
- 2026-08-05
Provisional, curator- or AI-assessed, and independently checkable. A reproduction outcome states what one attempt could reproduce — not a judgement of the authors.
Deep full-text extraction
Model: opusThe study tests whether a gene near the breakpoint of a balanced t(10;12) translocation in a Kallmann syndrome subject is involved in human puberty and, when mutated, causes idiopathic hypogonadotropic hypogonadism and Kallmann syndrome.
- ★ WDR11 is a gene involved in human puberty, identified via the chromosomal breakpoint of a balanced t(10;12) translocation in a Kallmann syndrome subject. finding
- ★ Heterozygous WDR11 missense mutations are found in patients with idiopathic hypogonadotropic hypogonadism and Kallmann syndrome. finding
- ★ Three alterations (A435T, R448Q, H690Q) affect WD domains important for β-propeller formation and protein-protein interaction. mechanism
- ★ WDR11 interacts with EMX1, a homeodomain transcription factor involved in the development of olfactory neurons. mechanism
- ★ WDR11 missense alterations reduce or abolish the WDR11-EMX1 interaction, suggesting impaired pubertal development results from deficiency of productive WDR11 protein interaction. mechanism
| Assay | System | Perturbation | Readout | Platform |
|---|---|---|---|---|
| translocation breakpoint mapping / cytogenetics | Kallmann syndrome patient with balanced t(10;12) translocation | none | chromosomal breakpoint location and candidate gene identification | — |
| mutation screening / gene sequencing | unrelated hypogonadal (IHH/Kallmann syndrome) subjects | none | heterozygous WDR11 missense mutations | — |
| protein-protein interaction assay | WDR11 and EMX1 proteins | WDR11 missense alterations (A435T, R448Q, H690Q, and others) | WDR11-EMX1 interaction (reduced or abolished) | — |
- – Six patients carried a total of five different heterozygous WDR11 missense mutations. 6 patients, 5 mutations
- – Three missense alterations (A435T, R448Q, H690Q) localize to WD domains important for β-propeller formation and protein-protein interaction.
- ▼ WDR11 missense alterations reduce or abolish WDR11 interaction with EMX1.
- count six patients (patients with WDR11 missense mutations)
- count five different heterozygous WDR11 missense mutations (distinct missense mutations identified)
- count three alterations (A435T, R448Q, H690Q) (mutations in WD domains important for β-propeller formation)
Statistical methods review
Model: sonnetA neutral, descriptive read of the statistical approach — what was done, and (for shared learning, not as criticism) what could also have been done.
The provided text is the article's front matter and abstract only (title, authors, affiliations, and a brief summary of findings about WDR11 mutations in Kallmann syndrome/hypogonadotropic hypogonadism). It does not include a Methods or Results section, so no statistical design, tests, or reporting details are stated in the text supplied.
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The provided text is limited to the title, author list, affiliations, and abstract, without a Methods or Results section describing the statistical analysis.↳ Could also: A review of the full Methods and Results sections (including any statistical analysis subsection, tables, and figure legends) would be needed to identify the specific tests, sample sizes, and reporting conventions used. — Providing the complete Methods/Results text would allow a fuller, evidence-based description of the study's statistical approach and any standard alternative methods relevant to its specific design (e.g., genotype-phenotype association analysis, protein-interaction assay comparisons).
What was reproduced
The exact results taken into scope, with each reported value next to the value our attempt produced.
Scope — pmid-20887964
Title: WDR11, a WD protein that interacts with transcription factor EMX1, is mutated in idiopathic hypogonadotropic hypogonadism and Kallmann syndrome. Journal: American Journal of Human Genetics, 2010. DOI: 10.1016/j.ajhg.2010.08.018 · PMID: 20887964 · PMCID: PMC2948809 Access: Not open access (Elsevier blocks full-text XML; abstract + metadata only via Europe PMC / NCBI E-utilities).
Reported results and their method classification
| # | Reported result | Method | In scope? |
|---|---|---|---|
| R1 | Chromosomal breakpoint of a balanced t(10;12) translocation in a Kallmann-syndrome subject maps to / disrupts the WDR11 region | Cytogenetics: FISH / breakpoint mapping (wet-lab) | No — wet-lab, manual |
| R2 | Six patients carry five different heterozygous WDR11 missense mutations (incl. A435T, R448Q, H690Q in WD/β-propeller domains) found by scanning the gene in unrelated hypogonadal subjects | Candidate-gene Sanger sequencing of a patient cohort (wet-lab) | No — wet-lab mutation discovery; no NGS/pipeline, no deposited variant dataset |
| R3 | WDR11 interacts with the homeodomain transcription factor EMX1 | Yeast two-hybrid screen (wet-lab) | No — wet-lab |
| R4 | The missense alterations reduce or abolish the WDR11–EMX1 interaction | Co-immunoprecipitation / GST pull-down interaction assays (wet-lab) | No — wet-lab functional assay |
| R5 | WDR11 / Emx1 expression pattern (development, olfactory neurons) | In situ hybridization / expression studies in model organisms (wet-lab) | No — wet-lab |
In-scope pipeline-derived results
None. No reported result is produced by a bioinformatic/computational pipeline. There is:
- no deposited computational dataset (no GEO / SRA / ENA / ArrayExpress / dbGaP / figshare / zenodo accession the paper relies on for a computational result);
- no analysis code / repository;
- no NGS, microarray, or array-CGH dataset to re-process;
- no in-silico pipeline output (e.g. an alignment/variant-calling/expression matrix) presented as a result.
The variant discovery (R2) is Sanger-based candidate-gene screening, not a sequencing pipeline that re-runs from raw reads; the few missense calls are reported in-text/supplementary tables, not as a reproducible computational artifact.
Outcome
DROP — non_pipeline. This is a classical wet-lab molecular-genetics +
functional-biology paper; there is no pipeline-derived computational result to
reproduce and no dataset/code to profile or re-run. No «our HPC» compute is
warranted. This is a well-founded drop (correct determination), not an our-side
failure.
Checked METHOD_CARDS.md — it contains only NGS pipeline recipes (bwa/samtools etc.), none relevant to this wet-lab paper.
Assessments & scoring basis
Each contributor’s verdict, the per-question basis, and the auditable, itemised worksheet behind it.
An automated assessment. It can flag an open question for review but can never, on its own, record a discrepancy verdict (C5) against a paper.
Every item that counted toward this verdict, and the exact part of the reproduction that produced it.
A PARTIAL with the same shape as a gene-discovery case report: the only in-scope computational claim — conservation of the three mutated residues — reproduced exactly (R395/H690/F1150 identical in 13/13 RefSeq orthologs via two independent aligners). The paper's central novelty is wet-lab/clinical (translocation breakpoint, 201-patient Sanger screen, Y2H/IP EMX1 interaction) plus proprietary MOE structural modeling, none of it deposited, so it is intrinsically non-reproducible. This sits on the data-availability/scope axis (q1 yellow self-defined ortholog sample; q4 wet-lab core not derivable), not a substantive discrepancy or fabrication signal, so the central claim is unverifiable (limited) rather than refuted.
Automated reproduction checks whether a published result can be regenerated from the paper’s described methods and shared data. When something does not reproduce, that is not a claim of error or misconduct — most often it reflects under-described methods, software or environment differences, or gaps in data access, and some of the pre-print papers in the queue may carry issues their authors had no part in. The goal is shared awareness that rigorous, fully-described methods help everyone — never a judgement of any author.
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Reproduction footprint
claude-opus-4-8Measured resources invested to assess this paper — sanitised (machine class only, no job ids/paths). Compute = HPC accounting (SLURM); tokens = the AI agent's session.