Abstract

Research in the Wilson lab centers on the three key components of nuclear lamina structure: lamins (encoded by LMNA, LMNB1, LMNB2), LEM-domain proteins (e.g., emerin, encoded by EMD), and BAF (Barrier to autointegration factor, encoded by BANF1). These proteins all bind each other directly, and are collectively required to organize and regulate chromatin, efficiently segregate chromosomes and rebuild nuclear structure after mitosis. Mutations in these proteins cause human ‘laminopathy’ diseases including Emery-Dreifuss muscular dystrophy (EDMD), cardiomyopathy, neuropathy, ‘accelerated aging’ (progeria syndromes), lipodystrophy/diabetes and metabolic syndrome. These disease mechanisms are not understood.

Current work aims to understand the molecular mechanisms of emerin function at the nuclear envelope, emerin molecular attachments to BAF/chromatin and lamin filaments, and how these interactions are controlled by metabolic status (O-GlcNAc cycle), phosphorylation, mechanical force and cell signaling. 

Most Welcome!

Einar Hallberg

Contact information

Professor Katherine Wilson, Department of Cell Biology, Johns Hopkins University School of Medicine, 725 N. Wolfe Street, G10 WBSB, Baltimore, MD 21205​