Identification of the DNA methylation signature of Mowat-Wilson syndrome.
Stefano Giuseppe CaraffiLiselot van der LaanKathleen RooneySlavica TrajkovaRoberta ZuntiniRaissa RelatorSadegheh HaghshenasMichael A LevyChiara BaldoGiorgia MandrileCarolyn LauzonDuccio Maria CordelliIvan IvanovskiAnna FettaElena Sukarova-AngelovskaAlfredo BruscoLisa PavinatoVerdiana PullanoMarcella ZollinoHaley McConkeyTartaglia MarcoGiovanni Battista FerreroBekim SadikovicLivia GaravelliPublished in: European journal of human genetics : EJHG (2024)
Mowat-Wilson syndrome (MOWS) is a rare congenital disease caused by haploinsufficiency of ZEB2, encoding a transcription factor required for neurodevelopment. MOWS is characterized by intellectual disability, epilepsy, typical facial phenotype and other anomalies, such as short stature, Hirschsprung disease, brain and heart defects. Despite some recognizable features, MOWS rarity and phenotypic variability may complicate its diagnosis, particularly in the neonatal period. In order to define a novel diagnostic biomarker for MOWS, we determined the genome-wide DNA methylation profile of DNA samples from 29 individuals with confirmed clinical and molecular diagnosis. Through multidimensional scaling and hierarchical clustering analysis, we identified and validated a DNA methylation signature involving 296 differentially methylated probes as part of the broader MOWS DNA methylation profile. The prevalence of hypomethylated CpG sites agrees with the main role of ZEB2 as a transcriptional repressor, while differential methylation within the ZEB2 locus supports the previously proposed autoregulation ability. Correlation studies compared the MOWS cohort with 56 previously described DNA methylation profiles of other neurodevelopmental disorders, further validating the specificity of this biomarker. In conclusion, MOWS DNA methylation signature is highly sensitive and reproducible, providing a useful tool to facilitate diagnosis.
Keyphrases
- dna methylation
- genome wide
- gene expression
- intellectual disability
- transcription factor
- epithelial mesenchymal transition
- long non coding rna
- single molecule
- heart failure
- autism spectrum disorder
- small molecule
- risk factors
- rna seq
- living cells
- oxidative stress
- single cell
- fluorescent probe
- subarachnoid hemorrhage
- functional connectivity
- genome wide association study