Dr Jordan Wright
Dr Jordan Wright
Contact
Email
show email address
Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID),...
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID),...
Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
Top Publications
- Bozaoglu, K, Massie, S, Irion, FE, Davies, KC, Kantor, I, Raabus, M, Haebich, KM, Vlahos, K, Howden, SE, Wright, J, et al. Simultaneous reprogramming and gene correction to generate six iPSC lines and isogenic controls from individuals with neurofibromatosis type 1.. Stem Cell Res 90: 103904 2026 view publication
- Wright, JL, Jiang, Y, Nayar, S, Rajeeve, V, Cutillas, PR, Li, H, Richardson, WD. The INO80 chromatin remodeling complex regulates histone H2A.Z mobility and the G1-S transition in oligodendrocyte precursors. 2026 view publication
- Tripathi, T, St John, M, Wright, J, Esber, N, Amor, DJ. Research Themes in KAT6A Syndrome: A Scoping Review. DNA 5(2) : 21 2026 view publication
- Wright, JL, Jiang, Y, Nayar, SG, Li, H, Richardson, WD. The INO80 Chromatin Remodeling Complex Regulates Histone H2A.Z Mobility and the G1-S Transition in Oligodendrocyte Precursors.. Glia 73(6) : 1307 -1323 2025 view publication
- Donoghue, S, Wright, J, Voss, AK, Lockhart, PJ, Amor, DJ. The Mendelian disorders of chromatin machinery: Harnessing metabolic pathways and therapies for treatment.. Mol Genet Metab 142(1) : 108360 2024 view publication
Page 1 of 3
Share //
