the proteasome implicated in anti-carcinogenic responses. Targeted-screening of pea germplasm has proven the utility of this approach in identifying sources of novel germplasm that would be difficult to detect by other means. The variant, JI 262, a wild Pisum elatius line originating from Turkey, revealed a deletion that was common to both TI1 and TI2, with a premature stop codon predicted for both proteins within the pre-propeptide region. The origin of such variation is intriguing, particularly as no other such variant was detected in the screening of 2822 Pisum lines. It is likely that the double mutation arose as a order THZ1-R consequence of a gene conversion event involving the two related TI genes, one of which had acquired the original deletion. As a consequence, JI 262 showed an extreme reduction in TIA and no CIA. In this work, despite having extremely small seeds and a thick black testa, JI 262 has been readily crossed with a cultivar and mutant progeny lines used to show that the mutation is linked with low TIA. This variant may progress into breeding programmes, where progeny lines can be selected on the basis of phenotypes , together with the molecular markers described here to follow the deletion. Beyond the opportunities for improved formulations for feed and food, and the higher inclusion of pea protein therein, the discovery of JI 262 opens possibilities for testing the function of TI proteins in seeds, and determining the extent to which these proteins contribute to plant and seed defence. The reductions in TIA/CIA achieved here for pea are higher than those obtained in soybean and have the advantage of being conferred by a genetically linked pair of mutant alleles. Studies in soybean have provided an alternative strategy for how seed protease inhibitor content may be manipulated. A soybean line expressing a mutant BBI transgene where both active sites have been interrupted with an inserted residue showed a significant reduction in the amount of seed inhibitor; TIA was reduced from 20 to 50 in seeds of the transgenic soybeans. The proposed explanation for the observed effects is that the more prevalent mRNA from the mutant gene, under the MI-77301 contro
