Functional characterization of androgen receptor dimerization interfaces [RNA-seq]

Although this mutant lost binding to many AR chromatin sites and attenuated the classical androgen-responsive transcriptome, it also retained activity at a subset of loci. In addition, it gained binding at new chromatin regions enriched for half-site androgen response elements and other transcription factor motifs. RUNX factors, whose binding motifs were among the enriched motifs, directly contributed to part of the altered AR program.

These data identify DBD dimerization as the principal determinant of canonical AR signaling, while revealing that monomeric DNA-binding of AR adopts alternative, cofactor-assisted chromatin-binding strategies.