D-2-hydroxyglutarate metabolism is linked to photorespiration in the shm1-1 mutant.

The Arabidopsis mutant shm1-1 is defective in mitochondrial serine hydroxymethyltransferase 1 activity and displays a lethal photorespiratory phenotype at ambient CO₂ concentration but grows normally at high CO₂. After transferring high CO₂-grown shm1-1 plants to ambient CO₂, the younger leaves remain photosynthetically active while developed leaves display increased yellowing and decreased F_V/ F_M values. Metabolite analysis of plants transferred from high CO₂ to ambient air indicates a massive light-dependent (photorespiratory) accumulation of glycine, 2-oxoglutarate (2 OG) and D-2-hydroxyglutarate ( D-2 HG). Amino acid markers of senescence accumulated in ambient air in wild-type and shm1-1 plants maintained in darkness and also build up in shm1-1 in the light. This, together with an enhanced transcription of the senescence marker SAG12 in shm1-1, suggests the initiation of senescence in shm1-1 under photorespiratory conditions. Mitochondrial D-2 HG dehydrogenase ( D-2 HGDH) converts D-2 HG into 2 OG. In vitro studies indicate that 2 OG exerts competitive inhibition on D-2 HGDH with a K_i of 1.96 m m. 2 OG is therefore a suitable candidate as inhibitor of the in vivo D-2HGDH activity, as 2 OG is produced and accumulates in mitochondria. Inhibition of the D-2 HGDH by 2 OG is likely a mechanism by which D-2HG accumulates in shm1-1, however it cannot be ruled out that D-2HG may also accumulate due to an active senescence programme that is initiated in these plants after transfer to photorespiratory conditions. Thus, a novel interaction of the photorespiratory pathway with cellular processes involving D-2HG has been identified. [ABSTRACT FROM AUTHOR]