The cohesin complex topologically encircles chromosomes and mediates sister 
chromatid cohesion to ensure accurate chromosome segregation upon cell division. 
Cohesin also participates in DNA repair and gene transcription. The 
Nipped-B-Mau2 protein complex loads cohesin onto chromosomes and the Pds5-Wapl 
complex removes cohesin. Pds5 is also essential for sister chromatid cohesion, 
indicating that it has functions beyond cohesin removal. The Brca2 DNA repair 
protein interacts with Pds5, but the roles of this complex beyond DNA repair are 
unknown. Here we show that Brca2 opposes Pds5 function in sister chromatid 
cohesion by assaying precocious sister chromatid separation in metaphase spreads 
of cultured cells depleted for these proteins. By genome-wide chromatin 
immunoprecipitation we find that Pds5 facilitates SA cohesin subunit association 
with DNA replication origins and that Brca2 inhibits SA binding, mirroring their 
effects on sister chromatid cohesion. Cohesin binding is maximal at replication 
origins and extends outward to occupy active genes and regulatory sequences. 
Pds5 and Wapl, but not Brca2, limit the distance that cohesin extends from 
origins, thereby determining which active genes, enhancers and silencers bind 
cohesin. Using RNA-seq we find that Brca2, Pds5 and Wapl influence the 
expression of most genes sensitive to Nipped-B and cohesin, largely in the same 
direction. These findings demonstrate that Brca2 regulates sister chromatid 
cohesion and gene expression in addition to its canonical role in DNA repair and 
expand the known functions of accessory proteins in cohesin's diverse functions.