Transcription initiation is a highly regulated process that determines gene expression outcomes1,2, yet the dynamics and efficiency of individual initiation events in living cells remain poorly understood. Here we combine endogenous tagging of human RNA polymerase II (Pol II) and the TFIID subunit TAF1 with dual-color live-cell single-molecule imaging to quantitatively map Pol II behavior during transcription initiation and early elongation. Using GRID (Genuine Rate Identification) analysis, we resolved four kinetic populations of chromatin-bound Pol II and find that more than 94% of promoter-bound molecules dissociate within tens of seconds, indicating globally inefficient initiation. Kinetic partitioning of Pol II dwell times into promoter-proximal pausing and gene body elongation reveals a global pausing index that is selectively increased by CDK9 inhibition. Single-cell analysis uncovers substantial heterogeneity in initiation efficiency and pausing that is not explained by cell-cycle state. Spatial heatmap analysis identifies recurrent Pol II ‘hotspots’, nuclear regions enriched for repeated long-lived Pol II binding events, whose abundance and architecture are selectively perturbed by inhibitors that trap Pol II at promoters or disrupt TFIID. Finally, acute depletion of TAF1 leaves initiation efficiency unchanged but significantly increases the pausing index and reduces elongation efficiency, consistent with impaired pause release. Together, these findings establish a general framework to quantify transcription efficiency in vivo and support a model in which TAF1, and by extension TFIID, promotes pause release and productive elongation.