HA-MSL2 wild-type and mutant ChIP-seq
The Male-specific Lethal (MSL) complex, particularly its core subunit MSL2, has been implicated in neurodevelopmental disorders (NDDs) through genetic studies, yet the functional consequences of patient-derived mutations remain poorly understood. To investigate how disease-associated MSL2 variants affect its chromatin binding, we performed chromatin immunoprecipitation sequencing (ChIP-seq) using HA-tagged wild-type and mutant MSL2 constructs overexpressed in HEK293T cells. This dataset enables genome-wide comparison of MSL2 occupancy between wild-type and mutant proteins, providing mechanistic insights into how specific amino acid changes disrupt MSL2-DNA interactions and potentially contribute to NDD pathogenesis.