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Background  The γ-aminubutyrate (GABA) shunt bypasses two steps of the tricarboxylic acid cycle, and is present in both prokaryotes and eukaryotes. In plants, the pathway is composed of the calcium/calmodulin-regulated cytosolic enzyme glutamate decarboxylase (GAD), the mitochondrial enzymes GABA transaminase (GABA-T; POP2) and succinic semialdehyde dehydrogenase (SSADH). We have previously shown that compromising the function of the GABA-shunt, by disrupting the  SSADH  gene of Arabidopsis, causes enhanced accumulation of reactive oxygen intermediates (ROIs) and cell death in response to light and heat stress. However, to date, genetic investigations of the relationships between enzymes of the GABA shunt have not been reported.    Principal Findings  To elucidate the role of succinic semialdehyde (SSA), γ-hydroxybutyrate (GHB) and GABA in the accumulation of ROIs, we combined two genetic approaches to suppress the severe phenotype of  ssadh  mutants. Analysis of double  pop2 ssadh  mutants revealed that  pop2  is epistatic to  ssadh . Moreover, we isolated EMS-generated mutants suppressing the phenotype of  ssadh  revealing two new  pop2  alleles. By measuring thermoluminescence at high temperature, the peroxide contents of  ssadh  and  pop2  mutants were evaluated, showing that only  ssadh  plants accumulate peroxides. In addition,  pop2 ssadh  seedlings are more sensitive to exogenous SSA or GHB relative to wild type, because GHB and/or SSA accumulate in these plants.    Significance  We conclude that the lack of supply of succinate and NADH to the TCA cycle is not responsible for the oxidative stress and growth retardations of  ssadh  mutants. Rather, we suggest that the accumulation of SSA, GHB, or both, produced downstream of the GABA-T transamination step, is toxic to the plants, resulting in high ROI levels and impaired development.

Mutants of GABA Transaminase (POP2) Suppress the Severe Phenotype of succinic semialdehyde dehydrogenase (ssadh) Mutants in Arabidopsis