The yellow seed trait is preferred by breeders for its potential to improve the seed quality and commercial value of Brassica napus.  In the present study, we produced yellow seed mutants using a CRISPR/Cas9 system when the two BnPAP2 homologs were knocked out.  Histochemical staining of the seed coat demonstrated that proanthocyanidin accumulation was significantly reduced in the pap2 double mutants and decreased specifically in the endothelial and palisade layer cells of the seed coat.  Transcriptomic and metabolite profiling analysis suggested that disruption of the BnPAP2 genes could reduce the expression of structural and regulated genes in the phenylpropanoid and flavonoid biosynthetic pathways.  The broad suppression of these genes might hinder proanthocyanidin accumulation during seed development, and thereby causing the yellow seed trait in B. napus.  These results indicate that BnPAP2 might play a vital role in the regulatory network controlling proanthocyanidin accumulation.