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Modification defects in the tRNA anticodon loop often impair yeast growth and cause human disease. In the budding yeast  Saccharomyces cerevisiae  and the phylogenetically distant fission yeast  Schizosaccharomyces pombe ,  trm7Δ  mutants grow poorly due to lack of 2'- O -methylation of C 32  and G 34  in the tRNA Phe  anticodon loop, and lesions in the human  TRM7  homolog  FTSJ1  cause non-syndromic X-linked intellectual disability (NSXLID). However, it is unclear why  trm7Δ  mutants grow poorly. We show here that despite the fact that  S .  cerevisiae trm7Δ  mutants had no detectable tRNA Phe  charging defect in rich media, the cells constitutively activated a robust general amino acid control (GAAC) response, acting through Gcn2, which senses uncharged tRNA. Consistent with reduced available charged tRNA Phe , the  trm7Δ  growth defect was suppressed by spontaneous mutations in phenylalanyl-tRNA synthetase (PheRS) or in the pol III negative regulator  MAF1 , and by overexpression of tRNA Phe , PheRS, or EF-1A; all of these also reduced GAAC activation. Genetic analysis also demonstrated that the  trm7Δ  growth defect was due to the constitutive robust GAAC activation as well as to the reduced available charged tRNA Phe . Robust GAAC activation was not observed with several other anticodon loop modification mutants. Analysis of  S .  pombe trm7  mutants led to similar observations.  S .  pombe  Trm7 depletion also resulted in no observable tRNA Phe  charging defect and a robust GAAC response, and suppressors mapped to PheRS and reduced GAAC activation. We speculate that GAAC activation is widely conserved in  trm7  mutants in eukaryotes, including metazoans, and might play a role in  FTSJ1 -mediated NSXLID.

Lack of 2'-O-methylation in the tRNA anticodon loop of two phylogenetically distant yeast species activates the general amino acid control pathway