Abstract
The evolutionarily conserved protein kinase complexes SnRK1 and TOR are central metabolic regulators essential for plant growth, development, and stress responses. They are activated by opposite signals, and the outcome of their activation is, in global terms, antagonistic. Similarly to their yeast and animal counterparts, SnRK1 is activated by the energy deficit often associated with stress to restore homeostasis, while TOR is activated in nutrient-rich conditions to promote growth. Recent evidence suggests that SnRK1 represses TOR in plants, revealing evolutionary conservation also in their crosstalk. Given their importance for integrating environmental information into growth and developmental programs, these signaling pathways hold great promise for reducing the growth penalties caused by stress. Here we review the literature connecting SnRK1 and TOR to plant stress responses. Although SnRK1 and TOR emerge mostly as positive regulators of defense and growth, respectively, the outcome of their activities in plant growth and performance is not always straightforward. Manipulation of both pathways under similar experimental setups, as well as further biochemical and genetic analyses of their molecular and functional interaction, is essential to fully understand the mechanisms through which these two metabolic pathways contribute to stress responses, growth, and development.
Highlights
IntroductionEnvironmental stresses such as extreme temperatures, drought, flooding, or attacks from various pathogens are major yieldlimiting factors, reducing crop productivity by >50% (Bray et al, 2000), and thereby our capacity to provide sufficient food, fiber, and fuel for a growing human population.To cope with adverse environmental conditions, plants trigger responses that range from rapid protective mechanisms (e.g. osmolyte accumulation) to developmental modifications (e.g. reduction in the shoot:root ratio), promoting stress tolerance and survival at the expense of growth
The evolutionarily conserved protein kinase complexes SnRK1 and TOR are central metabolic regulators essential for plant growth, development, and stress responses. They are activated by opposite signals, and the outcome of their activation is, in global terms, antagonistic. To their yeast and animal counterparts, SnRK1 is activated by the energy deficit often associated with stress to restore homeostasis, while TOR is activated in nutrient-rich conditions to promote growth
Environmental stresses such as extreme temperatures, drought, flooding, or attacks from various pathogens are major yieldlimiting factors, reducing crop productivity by >50% (Bray et al, 2000), and thereby our capacity to provide sufficient food, fiber, and fuel for a growing human population.To cope with adverse environmental conditions, plants trigger responses that range from rapid protective mechanisms to developmental modifications, promoting stress tolerance and survival at the expense of growth
Summary
Environmental stresses such as extreme temperatures, drought, flooding, or attacks from various pathogens are major yieldlimiting factors, reducing crop productivity by >50% (Bray et al, 2000), and thereby our capacity to provide sufficient food, fiber, and fuel for a growing human population.To cope with adverse environmental conditions, plants trigger responses that range from rapid protective mechanisms (e.g. osmolyte accumulation) to developmental modifications (e.g. reduction in the shoot:root ratio), promoting stress tolerance and survival at the expense of growth. Despite our increasing knowledge on stress responses, how stress impinges on growth is still poorly understood. A deep understanding of the interactions between stress and growth regulatory pathways is essential to uncouple the two processes, making the two features compatible in plant breeding and engineering strategies. 2262 | Margalha et al. In plants, there are two central nutrient-sensing kinases with increasing connections to stress responses and growth, and with largely antagonistic functions: the protein kinase complexes SnRK1 (Snf1-related protein kinase 1) and TOR (target of rapamycin) (Broeckx et al, 2016; Dobrenel et al, 2016a; Margalha et al, 2016; Baena-Gonzalez and Hanson, 2017; Shi et al, 2018). The SnRK1 and TOR pathways have been mostly studied independently and, despite an increasing interest, knowledge of their interconnections remains scarce. The answers to fundamental questions concerning their mutual regulation, as well as the mechanistic details behind commonly regulated processes, are still to be discovered
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