Kashyap Chhatbar

Dysfunction of a SET3-like complex underlies a family of related neurological disorders

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

Pervasive binding of the stem cell transcription factor SALL4 shapes the chromatin landscape

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

Tetramerisation governs SALL transcription factor function in development and disease

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

Modelling transcription with explainable AI uncovers context-specific epigenetic gene regulation at promoters and gene bodies

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.

A critique of the hypothesis that CA repeats are primary targets of neuronal MeCP2

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.

Neuronal non-CG methylation is an essential target for MeCP2 function

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.

SALL4 controls cell fate in response to DNA base composition

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.

Quantitative analysis questions the role of MeCP2 as a global regulator of alternative splicing

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.