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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Nat Chem Biol. 2014 Apr 28;10(6):450–456. doi: 10.1038/nchembio.1520

Figure 6. The BABA receptor IBI1 controls BABA-IR and plant growth suppression via separate pathways.

Figure 6

Binding of the R-enantiomer of BABA to the L-Asp-binding site of IBI1 blocks canonical aspartyl-tRNA synthetase (AspRS) activity, which primes the protein for pathogen-inducible defence activity in the cytoplasm (red). Concurrently, the inhibitory activity of R-BABA on AspRS activity leads to accumulation of uncharged tRNAs, which triggers GCN2-dependent phosphorylation of the translation initiation factor eIF2α and suppression of plant growth (blue).