GSK3 roles in stress responses

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Work in several plant species has implicated GSK3s in abiotic stress responses, although sometimes in conflicting ways [40,46,49-52] (Table 1). An up-regulation of GSK3 transcripts by salt stress has been reported in Arabidopsis (AtSK13, AtSK31 and AtSK42) [46], wheat (Triticum aestivum) (TaGSK1) [53], rice (OsGSK1) [40] and sugarcane (Saccharum officinarum) (SuSK) [52]. The above mentioned Arabidopsis GSKs are also induced by osmotic stress whereas rice OsGSK1 transcripts show a strong reduction following drought treatment [40]. Confirming the role of GSK3 as an active component of the salt stress signalling pathway, Arabidopsis plants overexpressing AtGSK1 (AtSK22) show a significant upregulation of several salt-stress-responsive genes, even in the absence of high salinity [49]. As a result, they exhibit an enhanced resistance to high salt conditions. In another study, a rice mutant with a T-DNA insertion in OsGSK1 exhibited elevated transcript levels of specific stress-responsive genes and a strong tolerance to high salt and drought treatments [40]. In Medicago sativa (alfalfa), the kinase activity of a plastid localized GSK3 (MsK4) was rapidly increased under hyperosmotic conditions [51]. The overexpression of MsK4 in Arabidopsis improved salt tolerance through changes in carbohydrate metabolism [51]. MsK4 is most similar to AtSK41, which does not respond to stress treatments [46]. However, AtSK31 shows a unique upregulation in plants that have been subjected to a dark period [46], making it a promising candidate for future studies.

GSK3s are also important in the plant response to biotic stress. M. sativa MsK1 shows a change in activity in response to plant defence elicitors. Interestingly, exposure to cellulase rapidly inhibited MsK1 activity and triggered its proteasome-dependent degradation [54]. The role of GSK3 in modulating the disease response was demonstrated when over-expression of MsK1 in Arabidopsis reduced the pathogen-mediated activation of AtMPK3 and AtMPK6 MAP kinases and exacerbated the susceptibility of the plant to Pseudomonas syringae [54]. This suggests that MsK1 acts as negative regulator of the basal defence response and that its elicitor-triggered regulation is essential to activate downstream components of plant defence pathways [54]. Another M. sativa GSK3, WIG (wound-induced gene), has a kinase activity that is transiently triggered following leaf injury [55]. Although none of the Arabidopsis GSKs seem to be transcriptionally induced by wounding [46], their kinase activity under mechanical injury has never been tested to date. Overall, GSK3 family members seem to have distinct regulatory functions and their activity appears to be modulated by various cues. How different stimuli modulate GSK3 activity during stress responses is largely unknown. One attractive hypothesis is that this occurs through phosphorylation/dephosphorylation by upstream components but this has yet to be demonstrated. Future research should also focus on isolating the targets of stress response-related GSK3s, which should open new possibilities in the quest for crop improvement.

The stress-responsive nature of GSK3s is evolutionarily ancient. GSK3 genes in the yeast Saccharomyces cerevisiae, particularly MCK1, are involved in responses to environmental stresses, including heat, cold, salt/osmotic stress, nutrient stress, oxidative stress and metal ion stress [56-58]. The temperature-sensitive phenotype of a yeast quadruple gsk3 mutant is rescued by expression of mammalian GSK3β [59], suggesting further cross-kingdom conservation of functionality. Similarly, Arabidopsis AtSK22 can rescue the salt-sensitive phenotype of the yeast mck1 mutant [60]. To thrive following transition from water to land, plants had to acquire new stress-tolerant adaptations, particularly in response to desiccation, light and temperature changes. For this reason, in the next section we consider the GSK3s of algae and of plants that evolved early to life on land.