1. Abnormalities in patterns of
tRNA methylation and in the activities of
tRNA methyltransferases are well-documented phenomena. In this study, we focused our attention on
tRNA from
adenocarcinoma, a 9,10-dimethyl-1,2-benzanthracene-induced mammary
tumor, because prior evidence has suggested the occurrence of an abnormal pattern of
tRNA methylation. 2. Chemical postlabeling of
tumor vs normal rat liver and mammary gland tRNAs revealed
tumor specific differences in the modified
nucleoside distribution, i.e., a 5.8-fold increase in
tumor N-2-methylguanosine together with a 2.7-, 2.8-, 2.6- and 2.8-fold decrease in
tumor 1-methyladenosine, dihydrouridine,
pseudouridine and 5-methylcytidyne, respectively. 3. Class A tRNAs, a slower gel migrating group of
tumor tRNAs, exhibited even lower
1-methyladenosine levels. Most of the remaining
nucleosides in class A tRNAs showed molar ratios similar to those found in bulk
tumor tRNA. However, N-2-methylguanosine levels in class A
tRNA are intermediate between bulk
tumor tRNA (2.8%) and mammary gland
tRNA (0.49%). 4. The only qualitative difference found in
tumor tRNA seems to be the absence of
inosine usually present in tRNAs from liver and mammary tissues. 5. In spite of its abnormal methylation pattern
adenocarcinoma tRNA binds to
glucocorticoid receptor protein from mouse AtT-20 cells, generating a 6S
tRNA-
protein complex, in a fashion similar to that previously described for the endogenous
tRNA isolated from the same cells.