Autophagy in Plants: Both a Puppet and a Puppet Master of Sugars.

Henry Christopher Janse Van Rensburg,Santiago Signorelli,Wim Van Den Ende

doi:10.3389/fpls.2019.00014

Henry Christopher Janse Van Rensburg, Santiago Signorelli + Show 1 more

Open Access

https://doi.org/10.3389/fpls.2019.00014

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Abstract

Autophagy is a major pathway that recycles cellular components in eukaryotic cells both under stressed and non-stressed conditions. Sugars participate both metabolically and as signaling molecules in development and response to various environmental and nutritional conditions. It is therefore essential to maintain metabolic homeostasis of sugars during non-stressed conditions in cells, not only to provide energy, but also to ensure effective signaling when exposed to stress. In both plants and animals, autophagy is activated by the energy sensor SnRK1/AMPK and inhibited by TOR kinase. SnRK1/AMPK and TOR kinases are both important regulators of cellular metabolism and are controlled to a large extent by the availability of sugars and sugar-phosphates in plants whereas in animals AMP/ATP indirectly translate sugar status. In plants, during nutrient and sugar deficiency, SnRK1 is activated, and TOR is inhibited to allow activation of autophagy which in turn recycles cellular components in an attempt to provide stress relief. Autophagy is thus indirectly regulated by the nutrient/sugar status of cells, but also regulates the level of nutrients/sugars by recycling cellular components. In both plants and animals sugars such as trehalose induce autophagy and in animals this is independent of the TOR pathway. The glucose-activated G-protein signaling pathway has also been demonstrated to activate autophagy, although the exact mechanism is not completely clear. This mini-review will focus on the interplay between sugar signaling and autophagy.

Highlights

Autophagy is a mechanism by which eukaryotic cells transport cellular components to lytic vacuoles where they are degraded and recycled
SnRK1 and TOR contribute to the major energy and/or stress dependent regulation of autophagy; new advances suggest that alternative pathways exist
Through SnRK1 and TOR, autophagy is regulated by sugar availability to recycle and provide the required resources for growth and development, and in turn autophagy assists in the removal of excess sugar from the cytosol, regulating the level of sugars available

Summary

INTRODUCTION

Autophagy is a mechanism by which eukaryotic cells transport cellular components to lytic vacuoles where they are degraded and recycled. The AMPK/Snf complex in animals and yeast regulates autophagy via at least two pathways, the first being through inhibiting TOR (Lee et al, 2010), preventing inhibition of autophagy, and secondly by directly phosphorylating ATG1, which activates autophagy (Wang et al, 2001; Egan et al, 2011; Kim J. et al, 2011). SnRK1 activates several downstream components such as the basic leucine zippers (bZIPs), the G-box binding factor (GBF5), bZIP11, and bZIP63 (BaenaGonzález et al, 2007; Delatte et al, 2011; Mair et al, 2015) These transcription factors control the expression of genes involved in catabolic pathways such as the degradation of cell walls, amino acids, protein, starch and initiation of autophagy to provide alternative sources of metabolites and energy under sugar starvation conditions (Baena-González et al, 2007). Autophagy seems to be key in seedling establishment, plant development and reproduction, potentially through RGS1 (Figure 2B)

AUTOPHAGY AND ROS HOMEOSTASIS UNDER OXIDATIVE STRESS

LINKS BETWEEN ALTERNATIVE SUGARS AND AUTOPHAGY

CONCLUDING REMARKS