Cajal body (CB) is a dynamic membrane-less nuclear hub enriched in factors essential for transcription apparatus, RNA chemical modifications, and ribonucleoprotein (RNP) assembly. My laboratory is interested in studying the molecular basis governing CB formation and how compromised CB can contribute to the pathogenesis of neuron degeneration, carcinogenesis, and other aging-related diseases.

CB formation is driven by liquid-liquid phase separation, nucleating disordered or IDR-containing proteins that have tendency to oligomerize and form a molecular condensate. In addition, CB forms non-randomly and is surrounded by genomic loci encoding RNAs, including snRNA of the spliceosome, TR of the telomerase, and histone mRNAs. We found disrupted CB integrity can lead to a plethora of molecular and cellular defects that are well-characterized hallmarks during human aging, including telomere attrition, histone depletion, loss of proteostasis, and mitochondrial dysfunction. In all, our research connects degenerative diseases with normal aging hallmarks, providing new druggable sites for degeneration and other aging-related symptoms.