Abstract：Many flowering plants possess a self-incompatibility system to prevent inbreeding. In Brassica oleracea, self-incompatibility is genetically controlled by S-locus cysteine rich protein (SCR) and S-locus receptor kinase (SRK). The SCR is the determinant of pollen S-haplotype specificity. In order to compare the structure of the gene and molecular characterization of the protein among the allelic SCRs, the nested PCR primers were designed on the basis of the conserved amino acids in the signal peptide's cleavage site and the ploy A of mRNA. Here we cloned partial cDNA sequence of SCR from six Brassica oleracea L.. Sequence analysis showed that the cDNA sequence of SCR in D3, E1, 240, A1, N1 and G1 were 319, 311, 290, 288, 385 and 377 bp, respectively, which all encompassed 3'UTR. Their coding regions predicted a protein of 58, 58, 58, 58, 58 and 55 amino acids, respectively. The protein sequences were identical between SCR-D3 and SCR3. SCR-E1, SCR-240, SCR-A1 and SCR-E1 also had the same sequences, and they were all identical to the SCR7. The SCR of G1 was a new S haplotype gene. Although SCR-E1, SCR-240, SCR-A1 and SCR-E1 were the same S haplotype, their 3'UTR were different. For example, the length, the polyadenylation signal and the adenine nucleotide's content were different among them. Sequencing and bioinformatic analysis indicated that there were some differences in the secondary structure and the 3-dimentional structure of the six SCRs, suggesting that the interactions of SCR with SRK required strict complementary space. All SCRs had potential phosphorylation sites, but no glycosylation sites. It showed that the phosphorylation of SCR might play roles in signal transduction of self-incompatibility. Furthermore, the amino acid residues interacting with SRK were situated on the surface of the SCR molecule, and most of these amino acid residues were basic amino acid. So, we suggested that the process of SCR interacting with SRK required the participation of the static charge. Hereby, we provided theoretically a new way for improving self-seed set by chemical reagent, such as neutral salts. Bioinformatic analysis also showed that the differences in the strength of self-incompatibility among different S haploids might be caused by their binding capacity of the SCR and the SRK. The differences in the strength of self-incompatibility among the same S haploids might be caused by the numbers of the SCR and the SRK. Moreover, the SCR were regulated at the mRNA level by the 3'UTR. The evolution speed of SCRs was fast, and the evolution speed of the 3'UTR was even faster than that of the coding regions. The results provide a theoretical basis for further research and utilization of self-incompatibility mechanism
