In order to prove that leucylated tRNA Ser CAGs actually participate in the translation process in Candida cells without such a rejection mechanism, we utilized a URA3 gene expression system derived from S.cerevisiae in C.maltosa, which was developed by Sugiyama et al. (1995) . Candida maltosa utilizes the codon CUG as serine and possesses the relevant tRNA Ser CAG gene (Sugiyama et al., 1995; Zimmer and Schunck, 1995) . Since the et al., 1995) . In the present study, this URA3 gene, with the CTG codon replaced by various leucine or serine codons, was utilized as a marker gene ( Figure 5A ). First, ADE1/ura3::C-ADE1) (Ohkuma et al., 1993) , the growth of which was monitored on minimal medium SD plates a plasmid in which the S.cerevisiae URA3 gene was inserted downstream of a C.maltosa-specific promoter in the presence and absence of uracil. When uracil was supplied to the SD plate for the (C-p) was constructed and designated as pCSU-CTG (Sugiyama, 1995) . As controls, mutant plasmids of pCSU-positive control experiments, all the transformants grew normally ( Figure 5B , middle row). However, in the absence CTG, in which the codon CTG was replaced by either the serine codon TCT or the leucine codon CTC, were of uracil, cells harboring pCCU and pCSU-CTC showed normal growth, whereas no growth was observed in those constructed and named pCSU-TCT and pCSU-CTC, respectively. In addition, a plasmid (pCCU) consisting of harboring pCSU-TCT and pUTH18 that contained no URA3 gene insertion. Cells harboring pCSU-CTG showed the URA3 gene of C.maltosa having a CTT leucine codon at the corresponding site, combined with the C.maltosa-weak but significant growth ( Figure 5B, uppermost row) . These results demonstrate that if the codon at position 45 specific promoter, was also used as a positive control. These variant plasmids were introduced into a URA3-is translated as leucine, active ODCase will be produced and the cells will be able to grow, but translation of the defective C.maltosa strain CHU1 (his5, ade1, ura3::C-codon with serine will produce inactive ODCase and the We believe that tRNA Ser CAG is the only molecule responsible for the leucine insertion corresponding to cells will be unable to grow. The result with cells harboring pCSU-CTG clearly demonstrates that the URA3 mutation codon CUG in C.maltosa cells, based on the following obervations. We have purified and sequenced a number on the C.maltosa chromosome was in some way complemented by the introduced pCSU-CTG plasmid, suggesting of leucine and serine tRNAs from Candida species, in which codon CUG is translated as serine, and failed in that the CTG codon was read at least partially as leucine in C.maltosa cells possessing tRNA Ser CAG.