Nodules provide the ideal environment for rhizobia to fix atmospheric nitrogen and convert it into a form plants can utilize. During nodulation it has been shown that there is an autoregulation of the number of nodules formed and that this involves a shoot derived signal. Recent work with brassinosteroid deficient mutants lk and lkb has shown that brassinosteroid deficiency in the shoot can reduce nodulation (Ferguson et al. 2005). Hence we examined whether brassinosteroids are involved in autoregulation of nodule numbers in pea (Pisum sativum L.). In order to identify the role of brassinosteroids in autoregulation double mutants were isolated from three crosses between lk and three non-allelic hypernodulating mutants, sym28, sym29 and nod3. Preliminary results suggest these double mutants possess a hypernodulating root phenotype even though lk is present. However even though double mutants appeared to hypernodulate they did not produce as many nodules as their hypernodulating parent, probably because the size of the root system was reduced. As double mutants from all three crosses hypernodulate it does not appear that brassinosteroids are necessary for hypernodulation. The result of further studies with these double mutants will be described in order to confirm the independence of brassinosteroid level and the autoregulation of nodulation.