Inhibition of transcription caused by DNA damage-impaired RNA polymerase II (Pol 
II) elongation conceals a local increase in de novo transcription, slowly 
progressing from Transcription Start Sites (TSSs) to gene ends. Although 
associated with accelerated repair of Pol II-encountered lesions and limited 
mutagenesis, it is still unclear how this mechanism is maintained during 
genotoxic stress-recovery. Here we uncover a widespread gain in chromatin 
accessibility and preservation of the active H3K27ac mark after UV-irradiation. 
The concomitant increase in Pol II escape from promoter-proximal pause (PPP) 
sites of most active genes, PROMPTs and enhancer RNAs favors unrestrained 
initiation, as evidenced by the synthesis of nascent RNAs including start RNAs. 
Accordingly, drug-inhibition of PPP-release replenishes levels of pre-initiating 
Pol II at TSSs after UV. Our data show that such continuous engagement of Pol II 
molecules ensures maximal transcription-driven repair throughout expressed genes 
and regulatory loci. Importantly, revealing this unanticipated regulatory layer 
of UV-response provides physiological relevant traction to the emerging concept 
that Pol II initiation rate is determined by pause-release dynamics.