Replication forks encounter impediments as they move through the genome, 
including natural barriers due to stable protein complexes and highly 
transcribed genes. Unlike lesions generated by exogenous damage, natural 
barriers are encountered in every S phase. Like humans, Schizosaccharomyces 
pombe encodes a single Pif1 family DNA helicase, Pfh1. Here, we show that Pfh1 
is required for efficient fork movement in the ribosomal DNA, the mating type 
locus, tRNA, 5S ribosomal RNA genes, and genes that are highly transcribed by 
RNA polymerase II. In addition, converged replication forks accumulated at all 
of these sites in the absence of Pfh1. The effects of Pfh1 on DNA replication 
are likely direct, as it had high binding to sites whose replication was 
impaired in its absence. Replication in the absence of Pfh1 resulted in DNA 
damage specifically at those sites that bound high levels of Pfh1 in wild-type 
cells and whose replication was slowed in its absence. Cells depleted of Pfh1 
were inviable if they also lacked the human TIMELESS homolog Swi1, a replisome 
component that stabilizes stalled forks. Thus, Pfh1 promotes DNA replication and 
separation of converged replication forks and suppresses DNA damage at 
hard-to-replicate sites.