Lysine represents a metabolic hub linking mitochondrial energy status with amino acid catabolism, yet its role in coordinating plant growth and development remains poorly characterised. The dapat mutant, which is deficient in L,L-diaminopimelate aminotransferase (DAPAT), exhibits severe growth inhibition associated with broad metabolic imbalance. This metabolic reprogramming is characterised by simultaneous depletion of carbohydrates (sugars and starch), and organic acids, accompanied by elevated amino acid pools, reflecting a profound disruption of carbon-nitrogen balance. These metabolic constraints coincide with altered expression of gibberellin (GA) biosynthetic genes (CPS, KS, GA3ox1), suggesting a potential link between lysine metabolism, energy status, and GA-mediated growth regulation. We therefore hypothesised that aberrant developmental defects in dapat arise from impaired GA metabolism. To test this hypothesis, we treated mutant plants with exogenous GA₃. Multivariate metabolomic analysis revealed a striking disconnect: GA restored the normal morphological phenotype of dapat but failed to correct the underlying metabolic dysfunction. GA-treated dapat plants maintain amino acid remobilisation despite growth restoration, as indicated by pronounced DIN6 induction, a marker of catabolic stress following energy starvation. These findings establish that lysine biosynthesis represents a critical metabolic constraint on plant development, and that growth hormone signalling can decouple morphological rescue from metabolic homoeostasis. This work exposes a fundamental mechanistic uncoupling between hormone-induced growth and energy balance in lysine-deficient plants, highlighting the critical role of lysine metabolism in integrating developmental and energetic cues.
Gouveia et al. (Thu,) studied this question.