Abstract
Post-translational modifications of the heptad repeat sequences in the C-terminal domain (CTD) of RNA polymerase II (Pol II) are well recognized for their roles in coordinating transcription with other nuclear processes that impinge upon transcription by the Pol II machinery; and this is primarily achieved through CTD interactions with the various nuclear factors. The identification of novel modifications on new regulatory sites of the CTD suggests that, instead of an independent action for all modifications on CTD, a combinatorial effect is in operation. In this review we focus on two well-characterized modifications of the CTD, namely serine phosphorylation and prolyl isomerization, and discuss the complex interplay between the enzymes modifying their respective regulatory sites. We summarize the current understanding of how the prolyl isomerization state of the CTD dictates the specificity of writers (CTD kinases), erasers (CTD phosphatases) and readers (CTD binding proteins) and how that correlates to transcription status. Subtle changes in prolyl isomerization states cannot be detected at the primary sequence level, we describe the methods that have been utilized to investigate this mode of regulation. Finally, a general model of how prolyl isomerization regulates the phosphorylation state of CTD, and therefore transcription-coupled processes, is proposed.
Highlights
The three RNA polymerases (Pol I, II, III) in eukaryotic systems have different transcriptional roles [1,2]
The C-terminal domain (CTD) is important as it acts as a scaffold that coordinates the polymerase II (Pol II) transcription process with other cellular events such as cell cycle regulation and DNA repair [4,5,6,7,8,9]
The recruitment of various regulatory factors to the CTD choreographs the progression of transcriptional initiation, pausing, elongation, mRNA co-processing and termination [12]
Summary
The three RNA polymerases (Pol I, II, III) in eukaryotic systems have different transcriptional roles [1,2]. Comprised of multiple heptad repeat sequences [3] is only found in Pol II [3]. The CTD is important as it acts as a scaffold that coordinates the Pol II transcription process with other cellular events such as cell cycle regulation and DNA repair [4,5,6,7,8,9]. The CTD consists of tandem repeats of the heptad consensus sequence. A minimal amount of repeats must be retained (usually around half of the normal number) by each species for cell viability, presumably by supporting transcription and its associated processes [11]
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