Abstract
Expression of Cystathionine γ-synthase (CGS), which catalyzes the key step of methionine biosynthesis in Arabidopsis thaliana, is regulated at the step of mRNA degradation in response to S-adenosyl-L-methionine (SAM). SAM induces translation arrest in cooperation with MTO1 region of CGS1 nascent peptide, which is followed by mRNA degradation. In order to elucidate this translation arrest mechanism, we analyzed arrested ribosome by chemical footprinting and UV crosslinking.
Consequently, translation arrest-specific signals were found at two sites in 26S rRNA. One is close to ribosomal protein L17, which constitutes narrowest region in the ribosome exit tunnel. This implies ribosomal protein L17 is involved in translation arrest. The other located in the P-site of peptidyl-transferase center and this change may induce translation arrest.
We are currently analyzing MTO1 region targets by introducing azide-tyrosine to MTO1 region as an UV crosslinker. How these changes and MTO1 region induce translation arrest will be discussed.
