With the aim at understanding the mechanism responsible for the low proliferative capacity of the adult pancreatic B-cell, expression of the "antiproliferative" gene retinoblastoma and that coding for p53 as well as certain genes coding for cyclin B1, cyclin D1 and p34cdc2 and p33cdk2 kinases, all of which are important for the cell cycle and mitosis, was assessed by the polymerase chain reaction in a semiquantitative assay. Islet expression of the p53 and retinoblastoma genes was higher than that of the liver, but lower or the same as that of the spleen, making expression of these genes an unlikely explanation for the low replicatory capacity of the B-cell. Similarly, islet expression of the genes coding for p33cdk2 kinase and cyclin D1 was not very different from that of the spleen. The levels of cyclin B1 mRNA and the mRNA coding for the p34cdc2 kinase were however both low in islets, compared with those of the spleen and the insulin-producing RINm5F cell line. Stimulation of B-cell proliferation did not change the expression of any of the genes studied. It is concluded that the low expression of cyclin B1 and p34cdc2 kinase and failure to induce these by stimulation of B-cell replication may play a role in maintaining adult B-cells in a state of low proliferative capacity.