Adrian Peter Bird

The paper identifies a dysfunction in the SET3-like complex involving TBLR1, ANKRD11, and SETD5 as a molecular basis for neurodevelopmental disorders.

This study shows MeCP2 binds methylated DNA in nucleosomes via linker DNA interactions beyond its canonical methyl binding domain, revealing a new mechanism for chromatin DNA methylation recognition.

This study shows SALL4 binds across the genome to shape chromatin and gene expression in stem cells.

This study identifies tetramerisation as essential for SALL transcription factor function, showing its role in DNA binding and linking it to developmental disorders.

The paper uses explainable AI to model transcriptional regulation, revealing context-specific epigenetic gene regulation at promoters and gene bodies using chromatin-associated protein data.

The paper identifies that C-terminal deletions in MECP2 cause Rett syndrome by reducing MeCP2 levels due to a specific reading frame shift, and shows a gene-editing strategy to correct this.

The paper investigates whether CA repeats are primary targets of MeCP2 and finds no evidence supporting this hypothesis, instead showing they contribute modestly to MeCP2-mediated gene expression.

The paper identifies shared proteomic and metabolic ontologies in Rett syndrome across species and validates them as potential biomarkers.

This study shows that MeCP2's binding to non-CG methylation, specifically mCAC trinucleotides, is critical for normal brain function, as demonstrated by severe Rett syndrome-like phenotypes in mice with a modified MeCP2 domain.

The paper identifies SALL4 as a protein that interprets DNA base composition by binding to AT-rich motifs, and shows its role in controlling cell fate through regulation of AT-rich gene expression.

This study uses machine learning to show that MeCP2 has minimal effects on alternative splicing across three systems and is indifferent to developmental DNA methylation changes.

The paper investigates the molecular effects of non-canonical MeCP2 mutations in neurons and mice, finding they impact known domains rather than causing new molecular mechanisms of Rett syndrome.

The paper shows MeCP2 binds to mCG and mCAC sequences in mouse brain, with binding density correlating with transcriptional regulation of neuronal genes.