Regulation of NSL by TAF4A is critical for genome stability and quiescence of muscle stem cells.

ABSTRACT: Acetylation of lamin A/C by the non-specific lethal complex, containing MOF and KANSL2, is instrumental for maintaining nuclear architecture and genome stability, but the mechanisms controlling expression of its components in different cell types are poorly characterized. Here, we show that TAF4A, primarily known as a subunit of TFIID, forms a complex with the heterotrimeric transcription factor NF-Y and is critical for cell type-specific regulation of Kansl2 in muscle stem cells. Inactivation of Taf4a reduces expression of Kansl2 and alters post-translational modification of lamin A/C, thereby decreasing nuclear stiffness, which disrupts the nuclear architecture and results in severe genomic instability. Reduced expression of Kansl2 in Taf4a-mutant muscle stem cells changes expression of

SUBMITTER: Georgieva AM 

PROVIDER: S-EPMC12484798 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature