Variant-specific disruption to notch signalling in PAX6 microphthalmia and aniridia patient-derived hiPSC optic cup-like organoids

The homeobox-containing transcription factor PAX6 is a key regulator of eye development. Pathogenic heterozygous PAX6 variants lead to variable ocular phenotypes, most commonly haploinsufficiency-induced aniridia. Missense variants are typically associated with milder ocular conditions, although variants in the DNA-binding paired domain which alter target binding lead to severe ocular phenotypes including bilateral microphthalmia, similar to SOX2-anophthalmia syndrome. However, the variant-specific pathway disruption resulting in phenotypic heterogeneity is not well understood. To investigate pathogenic mechanisms of PAX6 variants, transcriptomic and chromatin accessibility analysis was performed on hiPSC derived 3D optic cup-like organoids generated from patients with variants (i) PAX6<sup>N124K</sup> displaying combined microphthalmia, aniridia and optic nerve coloboma, and (ii) PAX6<sup>R261X</sup> exhibiting typical aniridia. Total RNA sequencing analysis revealed downregulation of SOX2 in missense PAX6<sup>N124K</sup> cups compared to both wildtype and PAX6<sup>R261X</sup> haploinsufficient aniridia controls, along with Notch signalling components and markers of proliferation and differentiation. Transcription factor binding motifs of Notch-related genes were also found to be differentially bound in PAX6<sup>N124K</sup> cups through ATACseq footprinting analysis. Our analysis of PAX6-related oculopathies using in vitro models reveals disruption to DNA binding perturbs SOX2 and Notch signalling, contributing to severe ocular phenotypes in patients with missense changes in the paired domain. This work reveals a previously unestablished role for PAX6 in SOX2 and Notch signalling regulation during early oculogenesis, as well as illuminating disease mechanisms underlying variant-specific ocular phenotypes and genotype-phenotype correlations. These novel insights can influence clinical care, and provide valuable data on potential therapeutic targets, which can guide future translational research.

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Publication Details

Journal
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Published
2025-04-23
DOI
https://doi.org/10.1016/j.bbadis.2025.167869
Citations
2
Primary Topic
Ocular Disorders and Treatments
Type
article
Field-Weighted Citation Impact
3.63

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article

Variant-specific disruption to notch signalling in PAX6 microphthalmia and aniridia patient-derived hiPSC optic cup-like organoids

Brian H. K. Chan, Philippa Harding, Dulce Lima Cunha, Nicholas Owen et al.
2 citations
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Ocular Disorders and Treatments
3.63
article

Variant-specific disruption to notch signalling in PAX6 microphthalmia and aniridia patient-derived hiPSC optic cup-like organoids

Brian H. K. Chan, Philippa Harding, Dulce Lima Cunha, Nicholas Owen, Joe Rainger, Mariya Moosajee, Jonathan Eintracht
article en
2 citations

Abstract

The homeobox-containing transcription factor PAX6 is a key regulator of eye development. Pathogenic heterozygous PAX6 variants lead to variable ocular phenotypes, most commonly haploinsufficiency-induced aniridia. Missense variants are typically associated with milder ocular conditions, although variants in the DNA-binding paired domain which alter target binding lead to severe ocular phenotypes including bilateral microphthalmia, similar to SOX2-anophthalmia syndrome. However, the variant-specific pathway disruption resulting in phenotypic heterogeneity is not well understood. To investigate pathogenic mechanisms of PAX6 variants, transcriptomic and chromatin accessibility analysis was performed on hiPSC derived 3D optic cup-like organoids generated from patients with variants (i) PAX6<sup>N124K</sup> displaying combined microphthalmia, aniridia and optic nerve coloboma, and (ii) PAX6<sup>R261X</sup> exhibiting typical aniridia. Total RNA sequencing analysis revealed downregulation of SOX2 in missense PAX6<sup>N124K</sup> cups compared to both wildtype and PAX6<sup>R261X</sup> haploinsufficient aniridia controls, along with Notch signalling components and markers of proliferation and differentiation. Transcription factor binding motifs of Notch-related genes were also found to be differentially bound in PAX6<sup>N124K</sup> cups through ATACseq footprinting analysis. Our analysis of PAX6-related oculopathies using in vitro models reveals disruption to DNA binding perturbs SOX2 and Notch signalling, contributing to severe ocular phenotypes in patients with missense changes in the paired domain. This work reveals a previously unestablished role for PAX6 in SOX2 and Notch signalling regulation during early oculogenesis, as well as illuminating disease mechanisms underlying variant-specific ocular phenotypes and genotype-phenotype correlations. These novel insights can influence clinical care, and provide valuable data on potential therapeutic targets, which can guide future translational research.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of DiseaseVol. 1871(6)
University College London (GB)
Wellcome Trust, National Institute for Health and Care Research, Moorfields Eye Charity, UCL Institute of Ophthalmology, University College London, National Institute for Health Research Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology
Zero hunger
Openalex Percentile: Top 8%
Ocular Disorders and Treatments
3.63
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