Abstract
Auxin, a phytohormone that affects almost every aspect of plant growth and development, is biosynthesized from tryptophan via the tryptamine, indole-3-acetamide, indole-3-pyruvic acid, and indole-3-acetaldoxime pathways. YUCCAs (YUCs), flavin monooxygenase enzymes, catalyze the conversion of indole-3-pyruvic acid (IPA) to the auxin (indole acetic acid). Arabidopsis thaliana YUC6 also exhibits thiol-reductase and chaperone activity in vitro; these activities require the highly conserved Cys-85 and are essential for scavenging of toxic reactive oxygen species (ROS) in the drought tolerance response. Here, we examined whether the YUC6 thiol reductase activity also participates in the delay in senescence observed in YUC6-overexpressing (YUC6-OX) plants. YUC6 overexpression delays leaf senescence in natural and dark-induced senescence conditions by reducing the expression of SENESCENCE-ASSOCIATED GENE 12 (SAG12). ROS accumulation normally occurs during senescence, but was not observed in the leaves of YUC6-OX plants; however, ROS accumulation was observed in YUC6-OXC85S plants, which overexpress a mutant YUC6 that lacks thiol reductase activity. We also found that YUC6-OX plants, but not YUC6-OXC85S plants, show upregulation of three genes encoding NADPH-dependent thioredoxin reductases (NTRA, NTRB, and NTRC), and GAMMA-GLUTAMYLCYSTEINE SYNTHETASE 1 (GSH1), encoding an enzyme involved in redox signaling. We further determined that excess ROS accumulation caused by methyl viologen treatment or decreased glutathione levels caused by buthionine sulfoximine treatment can decrease the levels of auxin efflux proteins such as PIN2-4. The expression of PINs is also reduced in YUC6-OX plants. These findings suggest that the thiol reductase activity of YUC6 may play an essential role in delaying senescence via the activation of genes involved in redox signaling and auxin availability.
Highlights
Plants undergo senescence to mobilize nutrients and remove unneeded organs
We previously showed that plants overexpressing YUC6, carrying the dominant mutant yuc6-1D, or transgenic for a 35S:YUC6 construct all exhibit delayed leaf senescence, along with extreme longevity (Kim et al, 2011)
To confirm that the delayed leaf senescence phenotype was caused by YUC6 overexpression at the molecular level, we examined the expression of a representative downstream gene, SENESCENCEASSOCIATED GENE 12 (SAG12), which is upregulated during senescence
Summary
Plants undergo senescence to mobilize nutrients and remove unneeded organs. Various phytohormones and environmental conditions interact to regulate senescence (Lim et al, 2007). Treatment with cytokinins or auxin delays senescence (Noodén et al, 1990; Kim et al, 2011). Detoxification systems such as antioxidant enzymes delay senescence (Ye et al, 2000; Lim et al, 2007). The developmental shift to senescence in plants is determined by the induction of Senescence-Associated Genes (SAGs), which are differentially expressed in response to treatment with phytohormones associated with senescence (Weaver et al, 1998; Gepstein et al, 2003)
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