Tat uses unexpected regulatory mechanisms to reprogram target immune cells to promote viral replication and rewire pathways beneficial for HIV.

CDK9 inhibition in human cells uncovers that Pol II pause duration regulates the frequency of productive transcription initiation.

The requirements for preinitiation complex formation/stability and transcription by RNA polymerase II in yeast cells are different from those in vitro, thereby altering the current view of basal transcription.

C. elegans equalizes the expression of X-chromosome genes between the sexes by reducing the recruitment of RNA polymerase II to promoters of X-linked genes in hermaphrodites, using a chromosome-restructuring complex called condensin.

The phosphorylation of tyrosine in the heptad repeat of the C-terminal domain of the largest subunit of RNA polymerase II promotes Ser2 phosphorylation by P-TEFb for pausing release.

The ATP-dependent chromatin remodeler Chd1 controls nucleosome turnover to allow RNA Polymerase to transcribe in vivo.

Histone variant H2A.Z is deposited near transcription start sites by the chromatin remodeler SWR1 and seems to be removed by RNA polymerase II at an early stage of transcription elongation.

Lysine mono- and di-methylation are two novel post-translational modifications of RNA polymerase II, which are enriched at promoters of active genes, precede lysine acetylation and mark early stages of transcription.

Quantification of all the major on- and off-pathway kinetic parameters in the transcription elongation cycle reveals that RNA polymerase II translocates slowly in a linear, non-branched Brownian ratchet mechanism.

Human cells respond to cytoplasmic mRNA depletion during early apoptosis by inhibiting RNA polymerase II transcription, thereby magnifying the gene expression shutdown during stress.