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Review
. 2011 Jan;155(1):2-18.
doi: 10.1104/pp.110.167569.

Ascorbate and glutathione: the heart of the redox hub

Christine H Foyer  1 , Graham Noctor
Affiliations
Review

Ascorbate and glutathione: the heart of the redox hub

Christine H Foyer et al. Plant Physiol. 2011 Jan.
No abstract available

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Figures

Figure 1.
Figure 1.
The chloroplast ascorbate-glutathione cycle as proposed in 1976. Scheme adapted from Foyer and Halliwell (1976).
Figure 2.
Figure 2.
Simple scheme illustrating the timeline of some important advances concerning ascorbate and glutathione during the development of concepts on the roles of ROS in plants since 1970. Purple text shows some of the many related advances in ROS metabolism that may not directly involve ascorbate or glutathione systems. References not cited in the text (in alphabetical order): Apostol et al., 1989; Conklin et al., 1996; Creissen et al., 1995; Davletova et al., 2005; Desikan et al., 1996, ; Doke, 1983; Edwards et al., 1990; Keller et al., 1998; Rizhsky et al., 2002; Takahashi et al., 1997; Wachter et al., 2005; Wheeler et al., 1998.
Figure 3.
Figure 3.
Redox potentials of NAD(P), glutathione, and ascorbate couples. Adapted from Noctor (2006). The shaded backgrounds indicate typical redox states in the absence of stress. For glutathione, the two curves indicate the relationship between reduction state and redox potential at total glutathione concentrations of 1 mm (triangles) and 5 mm (circles).
Figure 4.
Figure 4.
Interdependence and independence of glutathione and ascorbate in peroxide metabolism. The scheme is not meant to show an exhaustive inventory of all mechanisms. For further discussion, see text. ASC, Reduced ascorbate; MDHA(R), monodehydroascorbate (reductase); GST, glutathione S-transferase; ROH and ROOH, organic compound with alcohol and peroxide group, respectively.
Figure 5.
Figure 5.
Some possible glutathione-linked signaling mechanisms. GS-R, Glutathione S-conjugate; GSNOR, GSNO reductase; R, small organic molecule; SH, sulfhydryl (thiol) group; SSG, glutathionylated protein Cys residue. Other abbreviations as for Figure 4.
Figure 6.
Figure 6.
A schematic representation of possible interactions between ascorbate, ROS, and ABA. This scheme depicts the negative effects of the vtc1 and vtc2 mutations on the tissue ascorbate pool. A high level of tissue ascorbate will favor lower abundance of both ROS and ABA. However, a low ascorbate pool will favor increases in both ROS and ABA, together leading to an increase in signal transduction through ROS-mediated and ABA-dependent signaling cascades. The ABA signaling components have been placed in this scheme in relation to the control of growth, with ABI4 having a major downstream effect on the signaling cascade leading to the ascorbate-dependent repression of growth. The ABI1 and ABI2 protein phosphatases are involved in the transmission of ROS signals. For simplicity, in this scheme ABI3 and ABI5 have been placed downsteam of ABI1 and ABI2, but other interactions are also possible.
See this image and copyright information in PMC

References

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