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MYB  transcriptional elongation is regulated by an attenuator sequence within intron 1 that has been proposed to encode a RNA stem loop (SLR) followed by a polyU tract. We report that NFκBp50 can bind the SLR polyU RNA and promote  MYB  transcriptional elongation together with NFκBp65. We identified a conserved lysine-rich motif within the Rel homology domain (RHD) of NFκBp50, mutation of which abrogated the interaction of NFκBp50 with the SLR polyU and impaired NFκBp50 mediated  MYB  elongation. We observed that the TAR RNA-binding region of Tat is homologous to the NFκBp50 RHD lysine-rich motif, a finding consistent with HIV Tat acting as an effector of  MYB  transcriptional elongation in an SLR dependent manner. Furthermore, we identify the DNA binding activity of NFκBp50 as a key component required for the SLR polyU mediated regulation of  MYB . Collectively these results suggest that the  MYB  SLR polyU provides a platform for proteins to regulate  MYB  and reveals novel nucleic acid binding properties of NFκBp50 required for  MYB  regulation.

MYB Elongation Is Regulated by the Nucleic Acid Binding of NFκB p50 to the Intronic Stem-Loop Region