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Background  Cysteine is a component in organic compounds including glutathione that have been implicated in the adaptation of plants to stresses.  O -acetylserine (thiol) lyase (OAS-TL) catalyses the final step of cysteine biosynthesis. OAS-TL enzyme isoforms are localised in the cytoplasm, the plastids and mitochondria but the contribution of individual OAS-TL isoforms to plant sulphur metabolism has not yet been fully clarified.    Results  The seedling lethal phenotype of the  Arabidopsis onset of leaf death3-1  ( old3-1 ) mutant is due to a point mutation in the  OAS-A1  gene, encoding the cytosolic OAS-TL. The mutation causes a single amino acid substitution from Gly 162  to Glu 162 , abolishing old3-1 OAS-TL activity  in vitro . The  old3-1  mutation segregates as a monogenic semi-dominant trait when backcrossed to its wild type accession Landsberg  erecta  (L er -0) and the Di-2 accession. Consistent with its semi-dominant behaviour, wild type L er -0 plants transformed with the mutated  old3-1  gene, displayed the early leaf death phenotype. However, the  old3-1  mutation segregates in an 11:4:1 (wild type: semi-dominant: mutant) ratio when backcrossed to the Colombia-0 and Wassilewskija accessions. Thus, the early leaf death phenotype depends on two semi-dominant loci. The second locus that determines the  old3-1  early leaf death phenotype is referred to as  odd-ler  (for   o l d 3   d eterminant in the L er  accession) and is located on chromosome 3. The early leaf death phenotype is temperature dependent and is associated with increased expression of defence-response and oxidative-stress marker genes. Independent of the presence of the  odd-ler  gene,  OAS-A1  is involved in maintaining sulphur and thiol levels and is required for resistance against cadmium stress.    Conclusions  The cytosolic OAS-TL is involved in maintaining organic sulphur levels. The  old3-1  mutation causes genome-dependent and independent phenotypes and uncovers a novel function for the mutated OAS-TL in cell death regulation.

A mutation in the cytosolic O-acetylserine (thiol) lyase induces a genome-dependent early leaf death phenotype in Arabidopsis