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

Reza Shirzadian-Khorramabad, Hai-Chun Jing, Gerja E. Everts, Jos H. M. Schippers, Jacques Hille, Paul P. Dijkwel*

*Corresponding author for this work

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    Abstract

    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 semidominant trait when backcrossed to its wild type accession Landsberg erecta (Ler-0) and the Di-2 accession. Consistent with its semi-dominant behaviour, wild type Ler-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 old3 determinant in the Ler 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.

    Original languageEnglish
    Article number80
    Number of pages12
    JournalBMC Plant Biology
    Volume10
    Issue number1
    DOIs
    Publication statusPublished - 29-Apr-2010

    Keywords

    • ACETYLTRANSFERASE GENE FAMILY
    • CYSTEINE SYNTHASE COMPLEX
    • MAP-BASED CLONING
    • SERINE ACETYLTRANSFERASE
    • O-ACETYLSERINE(THIOL)LYASE GENE
    • AMINO-ACIDS
    • GLUTATHIONE HOMEOSTASIS
    • FUNCTIONAL-ANALYSIS
    • SULFUR METABOLISM
    • CADMIUM TOLERANCE

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