Catalytic subunit of the CTDK-I complex, which hyperphosphorylates the C-terminal heptapeptide repeat domain (CTD) of the largest RNA polymerase II subunit. Involved in RNA polymerase II transcriptional elongation and pre-mRNA 3'-end processing (By similarity). Together with ctk2/lsc1, required for the regulation of cytokinesis by phosphorylating 'Ser-2' residues found in the heptad repeats of the CTD. Required for nuclear localization of ctk2/lsc1. Positively regulates the septation initiation network (SIN) and promotes successful completion of cytokinesis in response to perturbation of the actomyosin ring. Acts in parallel to clp1 to promote actomyosin ring stability upon cytokinesis checkpoint activation. [DNA-directed RNA polymerase] + ATP = ADP + H(+) + phospho-[DNA-directed RNA polymerase] CTDK-I consists of three subunits, ctk1/lsk1, ctk2/lsc1 and ctk3 (also called alpha, beta and gamma) (By similarity). Interacts with ctk2/lsc1. This interaction is dependent on kinase activity. Localized to nucleus during all cell cycle phases. Cells display severe cytokinesis defects. They are able to form, but not maintain the integrity of the actomyosin ring and are unable to successfully complete division septum formation upon treatment with low doses (0.3 uM) of actin depolymerizing drug, latrunculin A (LatA). However, deletion mutants are competent to delay nuclear cycle progression after cytokinetic failure upon treatment with LatA. In addition, deletion mutants suppress the lethal, multiseptate phenotype conferred by hyperactivation of the SIN. Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily.