Disponibile in Tedesco

Redox adjustments are central to most stress responses. However, little is known about the mechanisms of how the antioxidant system is regulated by cellular signalling to counteract oxidative stress. High soil salinity is a major environmental constraint for plant growth and development. Salinity imposes a water-deficit as well as ion stress, which causes damaging effects including an over-production of reactive oxygen species (ROS). Glucose-6-phosphate dehydrogenase (G6PD) catalyzes a key step of the oxidative pentose phosphate pathway which provides NADPH for reductive biosynthesis and maintenance of cellular redox state. G6PD deficiency is the most common enzymopathy in humans, affecting millions of people worldwide. In plants, G6PD activity is present in plastids and the cytosol however, its role during stress is unclear. The activity of G6PD is tightly controlled: phosphorylation has been proposed as a regulational mechanism in animals and plants. Glycogen synthase kinase 3 (GSK3) constitutes a class of evolutionary conserved serine/threonine kinases. Originally identified in mammals as a glycogen metabolism modulator, GSK3 is now recognized as a central regulator of an array of cellular events in many organisms. In plants, GSK3/Shaggy-like kinases have been proposed to have different roles during physiological stress responses. Analysis of the in vivo kinase activity of ASK5, an Arabidopsis GSK3/Shaggy-like kinase, showed that ASK5 activity is stimulated by salinity stress. Loss of ASK5 led to accumulation of high H2O2 levels in response to prolonged stress and rendered plants hypersensitive to high salinity, whereas plants with enhanced ASK5 activity showed low levels of H2O2 upon stress and improved salt stress tolerance. Moreover, plants overexpressing ASK5 showed a better performance also upon other abiotic as well as biotic stresses. To follow up on the idea that ASK5 might impact on cellular redox state upon stress by regulating the activity of metabolic enzymes, a robot-based screen for multiple enzymatic activities was performed. This and other more targeted analysis revealed that stress-induced stimulation of G6PD is impaired in ask5 mutants but enhanced in ASK5-overexpressing plants. Significantly, our subsequent studies identified G6PD as an in vitro and in vivo substrate of ASK5. Particularly, ASK5 directs its activity towards G6PD on an evolutionary conserved threonine residue, thereby enhancing the enzyme activity. A phosphomimicking mutagenized enzyme showed a constitutive enhanced activity in vivo.

The role of GSK-3 kinases in Arabidopsis thaliana stress response

DAL SANTO, SILVIA
2009-01-01

Abstract

Redox adjustments are central to most stress responses. However, little is known about the mechanisms of how the antioxidant system is regulated by cellular signalling to counteract oxidative stress. High soil salinity is a major environmental constraint for plant growth and development. Salinity imposes a water-deficit as well as ion stress, which causes damaging effects including an over-production of reactive oxygen species (ROS). Glucose-6-phosphate dehydrogenase (G6PD) catalyzes a key step of the oxidative pentose phosphate pathway which provides NADPH for reductive biosynthesis and maintenance of cellular redox state. G6PD deficiency is the most common enzymopathy in humans, affecting millions of people worldwide. In plants, G6PD activity is present in plastids and the cytosol however, its role during stress is unclear. The activity of G6PD is tightly controlled: phosphorylation has been proposed as a regulational mechanism in animals and plants. Glycogen synthase kinase 3 (GSK3) constitutes a class of evolutionary conserved serine/threonine kinases. Originally identified in mammals as a glycogen metabolism modulator, GSK3 is now recognized as a central regulator of an array of cellular events in many organisms. In plants, GSK3/Shaggy-like kinases have been proposed to have different roles during physiological stress responses. Analysis of the in vivo kinase activity of ASK5, an Arabidopsis GSK3/Shaggy-like kinase, showed that ASK5 activity is stimulated by salinity stress. Loss of ASK5 led to accumulation of high H2O2 levels in response to prolonged stress and rendered plants hypersensitive to high salinity, whereas plants with enhanced ASK5 activity showed low levels of H2O2 upon stress and improved salt stress tolerance. Moreover, plants overexpressing ASK5 showed a better performance also upon other abiotic as well as biotic stresses. To follow up on the idea that ASK5 might impact on cellular redox state upon stress by regulating the activity of metabolic enzymes, a robot-based screen for multiple enzymatic activities was performed. This and other more targeted analysis revealed that stress-induced stimulation of G6PD is impaired in ask5 mutants but enhanced in ASK5-overexpressing plants. Significantly, our subsequent studies identified G6PD as an in vitro and in vivo substrate of ASK5. Particularly, ASK5 directs its activity towards G6PD on an evolutionary conserved threonine residue, thereby enhancing the enzyme activity. A phosphomimicking mutagenized enzyme showed a constitutive enhanced activity in vivo.
2009
Arabidopsis; G6PD; stress response; GSK-3 Shaggy kinase
Disponibile in Tedesco
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/345259
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