Evidence map›Paper›PMID 40855817›Full record

ArticleDisease models & mechanisms2025

Models of Bosch-Boonstra-Schaaf optic atrophy syndrome reveal genotype-phenotype correlations in brain structure and behavior.

Johann G Maass, Dominik Kamionek, Annabelle Mantilleri, Susanne Theiss, Laura Dötsch, Felix Franke, Tim Schubert, Jonas G Scheck, Claudia Pitzer, Paolo Piovani and 7 more

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Johann G MaassInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.ORCID 0009-0006-2069-5470
Dominik KamionekInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.ORCID 0009-0008-3878-2366
Annabelle MantilleriInstitute of Biology Valrose (iBV), University Côte d'Azur (UCA), CNRS 7277, Inserm 1091, Avenue Valrose 28, Nice 06108, France.
Susanne TheissInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.
Laura DötschInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.
Felix FrankeInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.ORCID 0009-0006-1696-3030
Tim SchubertInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.ORCID 0009-0003-1696-4402
Jonas G ScheckNeuroradiology Department, University Hospital Heidelberg, 69120 Heidelberg, Germany.ORCID 0009-0002-7872-2831
Claudia PitzerInterdisciplinary Neurobehavioral Core, Heidelberg University, 69120 Heidelberg, Germany.
Paolo PiovaniInstitute of Biology Valrose (iBV), University Côte d'Azur (UCA), CNRS 7277, Inserm 1091, Avenue Valrose 28, Nice 06108, France.
Michele BertacchiInstitute of Biology Valrose (iBV), University Côte d'Azur (UCA), CNRS 7277, Inserm 1091, Avenue Valrose 28, Nice 06108, France.ORCID 0000-0002-4402-4974
Olivier DeschauxInstitute of Biology Valrose (iBV), University Côte d'Azur (UCA), CNRS 7277, Inserm 1091, Avenue Valrose 28, Nice 06108, France.
Anubhav SinghInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.
Chun-An ChenDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Henning FröhlichInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.
Michèle StuderInstitute of Biology Valrose (iBV), University Côte d'Azur (UCA), CNRS 7277, Inserm 1091, Avenue Valrose 28, Nice 06108, France.ORCID 0000-0001-7105-2957
Christian P SchaafInstitute of Human Genetics, Heidelberg University Clinic, 69120 Heidelberg, Germany.ORCID 0000-0002-2148-7490

Funding

Deutsche Forschungsgemeinschaft 532002382ERA-Net NEURON ANR- 21-NEU2-0003-03ERA-NET Neuron ANR- 21-NEU2-0003-03Fondation de France 00123416Fondation de France #00154573Fondation de France 00154573Fondation pour la Recherche Medicale EQU202003010222Fondation pour la Recherche Médicale EQU202003010222German Neurology SocietyInstitut Clinique de la SourisPHENOMINUniversitätsklinikum Heidelberg
6 · The paper itself

Abstract

Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is a rare, autosomal dominant neurodevelopmental disorder caused by pathogenic variants in NR2F1, characterized by developmental delay, intellectual disability, optic nerve anomalies and autism spectrum disorder. Most pathogenic variants cluster within the highly conserved DNA-binding domain (DBD) or ligand-binding domain (LBD) of NR2F1 and are associated with variable clinical severity, suggesting a genotype-phenotype correlation. Although previous mouse models have provided important insights, comprehensive behavioral characterization remains limited. Here, we present two novel BBSOAS mouse models harboring patient-specific variants in the DBD (Nr2f1+/R139L) and LBD (Nr2f1+/E397*), alongside the established Nr2f1+/- model. We analyzed brain morphology and behavior to further expand the murine phenotype and investigate the genotype-phenotype correlation. We demonstrate that these models recapitulate key aspects of the BBSOAS phenotype, including deficits in cognition, social communication and motor function, and that the presence and severity of behavioral abnormalities are dependent on variant type. Our findings provide new evidence for a genotype-phenotype correlation associated with domain-specific NR2F1 variants and establish a robust platform for future mechanistic and therapeutic studies.

Indexed as

Behavior, AnimalBrainGenetic Association StudiesOptic AtrophyAnimalsCOUP Transcription Factor IDisease Models, AnimalFemaleHumansMaleMiceMice, Inbred C57BLPhenotypeCOUP Transcription Factor INR2F1 protein, humanASDAutismBBSOASBosch-Boonstra-Schaaf optic atrophy syndromeNeurodevelopmental disorderNR2F1Social behavior

Identifiers

PMID40855817
PMCPMC12505268

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.