It is well established that eukaryotic genomes are pervasively transcribed 
producing cryptic unstable transcripts (CUTs). However, the mechanisms 
regulating pervasive transcription are not well understood. Here, we report that 
the fission yeast CENP-B homolog Abp1 plays an important role in preventing 
pervasive transcription. We show that loss of abp1 results in the accumulation 
of CUTs, which are targeted for degradation by the exosome pathway. These CUTs 
originate from different types of genomic features, but the highest increase 
corresponds to Tf2 retrotransposons and rDNA repeats, where they map along the 
entire elements. In the absence of abp1, increased RNAPII-Ser5P occupancy is 
observed throughout the Tf2 coding region and, unexpectedly, RNAPII-Ser5P is 
enriched at rDNA repeats. Loss of abp1 also results in Tf2 derepression and 
increased nucleolus size. Altogether these results suggest that Abp1 prevents 
pervasive RNAPII transcription of repetitive DNA elements (i.e., Tf2 and rDNA 
repeats) from internal cryptic sites.