Glutathione in plant biotic interactions

Glutathione in plant biotic interactions

metabolism. Unlike nuclear GSH sequestration at G1, which altered the expression of genes associated with auxin transport, whole cell GSH depletion in...

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metabolism. Unlike nuclear GSH sequestration at G1, which altered the expression of genes associated with auxin transport, whole cell GSH depletion in rml1 specifically altered transcripts encoding auxin signaling components. Root glutathione levels were maintained when auxin transport was inhibited by strigolactones or N-1-naphthylphthalamic acid. Moreover, strigolactone signaling through the MAX2 pathway sensitized lateral root development to GSH depletion. These data provide evidence of a cycle of reciprocal control of auxin and redox functions in cell cycle progression and root meristem development that provides a conceptual framework to understand how redox signals regulate plant growth with a contribution from plastid to nucleus signaling of thiol status. Keywords: Glutathione, Cell Cycle, Hormones, Gene expression doi:10.1016/j.freeradbiomed.2012.08.141 Symp. 16.4

Glutathione in plant biotic interactions A. Puppo*1, P. Frendo1 1 Université de Nice - Sophia Antipolis, France, 2Centre National de la Recherche Scientifique, France Legumes form a symbiotic interaction with soil bacteria of the Rhizobiaceae family to produce nitrogen-fixing root nodules. Genetic approaches using a nodule nitrogen-fixing zone specific promoter were employed to determine the importance of glutathione (GSH) and homoglutathione (hGSH) in biological nitrogen fixation (BNF) of the Medicago truncatula – Sinorhizobium meliloti symbiosis. Down-regulation of the γglutamylcysteine synthetase (γECS) gene by RNA interference resulted in significantly lower BNF and a reduction in the nodule size. Conversely, γECS overexpression was correlated with increased BNF. These data show that the plant (h)GSH content of the nodule nitrogen-fixing zone modulates the efficiency of the BNF process. Based on the link established by glutaredoxins (Grx) between free GSH and protein post-translational modifications, we investigated the contribution of the three Grx-encoding genes present in the S. meliloti genome to the symbiotic process; grx1 and grx2 mutations decreased the growth of the free-living bacteria and the nitrogen fixation capacity of bacteroids, the symbiotic form of bacteria. Mutation of grx1 led to nodule abortion and an absence of bacteroid differentiation, whereas grx2 mutation decreased nodule development. Thus, the two S. meliloti Grx are essential for BNF.

On the other hand, (h)GSH were also found to be important for the success of root-knot nematode (a plant parasitic worm) infection in M. truncatula. (h)GSH metabolism in neoformed gall organs differs from that in uninfected roots. Depletion of (h)GSH content impaired nematode egg mass formation and modified the sexratio. A substantial modification of starch and gaminobutyrate metabolism and of malate and glucose content was observed in (h)GSH-depleted galls. Thus, (h)GSH appear to have a key role in the regulation of giant cell metabolism. Taken together, these results highlight the importance of (h)GSH in M. truncatula biotic interactions. Keywords: Glutathione, Legumes, Symbiosis, Pathogenesis doi:10.1016/j.freeradbiomed.2012.08.142 Symp. 16.5

Compensatory gene expression in gluthathione deficient mice: implications for ageing and disease susceptibility T.J. Kavanagh, University of Washington, USA The tripeptide thiol glutathione (GSH) is an important intracellular antioxidant and free racial scavenger. Glutathione synthesis is carried out in two ATPdependent steps, the first of which is catalyzed by the enzyme glutamate cysteine ligase (GCL), a heterodimeric enzyme composed of catalytic (GCLC) and modifier (GCLM) subunits. We have generated mice in which Gclm has been genetically disrupted (Gclm null mice). These mice have approximately 10 - 20% of normal levels of GSH in most of their tissues. This lack of GSH has major effects on gene expression, especially in the liver, resulting in changes in alternative antioxidant responses, fat metabolism, and susceptibility to drug and toxicant-induced oxidative stress. Moreover, responsiveness to agents that induce inflammation is severely perturbed, as is vascular reactivity, a process especially sensitive to redox status. Because there are relatively common polymorphisms in GCLC and GCLM genes in human populations, this mouse model of compromised GSH synthesis has value for predicting the effects of compromised GSH synthesis in human diseases associated with oxidative stress and aging. doi:10.1016/j.freeradbiomed.2012.08.143

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