A mutation in the cytosolic O-acetylserine (thiol) lyase induces the genome-dependent old3-1 early leaf death phenotype in Arabidopsis
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چکیده
The Arabidopsis onset of leaf death3-1 (old3-1) mutant shows a temperature dependent premature leaf death phenotype. The old3-1 mutation segregates as a monogenic co-dominant trait when backcrossed to its wild type accession Landsberg erecta (Ler-0). In contrast, F2 progeny of old3-1 backcrossed to Col-0 segregates in an 11:4:1 (wild type: co-dominant: mutant) ratio demonstrating that the early leaf death phenotype depends on two loci. The second locus that determines the old3-1 early leaf death phenotype is referred to as ODD (for old3 determination). The old3-1 mutation is caused by a point mutation in the cytosolic O-acetylserine (thiol) lyase OAS-TL gene causing a single amino acid change from Gly to Glu. OAS-TL enzymes catalyse the formation of cysteine and mitochondrial and plastidic OAS-TL enzymes are believed to contribute primarily to cysteine biosynthesis as well. The old3-1 protein has no detectable in vitro OAS-TL activity. In order to distinguish the direct effects of the mutated OAS-TL we isolated a T-DNA insertional OAS-TL mutant and designated as old3-2. The cytosolic OAS-TL was found to function in providing resistance against cadmium-induced stress and for maintaining sulphur and thiols levels, independent of the ODD gene. The old3-1 early leaf death phenotype is associated with high expression of defence response and oxidative stress marker genes. Further analysis placed the ODD gene within a ~ 50-kb genome region on chromosome 3 which carries a recently integrated copia-like retrotransposon gene that is present in the Ler-0, but not in the Col-0 genome. The insertion is associated with a high genetic diversity including SNPs, insertions/deletions and altered gene structures. Thus, the old3-1 mutation causes genome dependent and independent
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