OXIDATIVE STRESS AND AUTOPHAGY IN PLANT CELLS: THE ROLE OF MITOCHONDRIA

Original title

ОКИСЛИТЕЛЬНЫЙ СТРЕСС И АУТОФАГИЯ В КЛЕТКАХ РАСТЕНИЙ: РОЛЬ МИТОХОНДРИЙ

Authors

F.V. Minibayeva1,2

Contact information

¹KIBB, FRC Kazan Scientific Center of RAS

²KFU, Kazan, e-mail Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра.

Pages

65-65

DOI

10.31255/978-5-94797-318-1-65-65

Abstract

Accumulation of reactive oxygen and nitrogen species (ROS and RNS) is a universal marker of stress in the cells of living organisms. A tight link exists between metabolic and signalling path-ways that control the redox status, energy metabolism and autophagy in plants affected by stress. Autophagy is an evolutionary conserved pathway that degrades oxidized, damaged and malfunc-tioning cellular macromolecules and organelles. In eukaryotes, autophagic degradation is neces-sary for maintenance of metabolic homeostasis, support of immunity and viability of an organism. In 2016, Yoshinori Ohsumi was awarded the Nobel Prize in physiology and medicine for his dis-coveries in the mechanisms of autophagy. Despite the great progress achieved in the studies of autophagy mechanisms in yeasts and mammals, our understanding of how this process functions in plants remains very limited. This is because of the complexity of plant genomes, the differences in biochemical processes, and the great diversity of metabolites and defence mechanisms of plants that occur due to their autotrophy and attached life style. Here we demonstrate that in wheat plants abiotic stresses such as oxidative, nitrosative and temperature stresses, as well as wounding and desiccation, all induce the formation of autophagic vesicles (autophagosomes) and upregulate the autophagic genes TaATG4, TaATG6, TaATG8. A decrease in mitochondrial membrane poten-tial and a lowering in cellular energy status accompany these processes. It is also shown that when plants are exposed to aggressive prooxidants, mitochondria can become a target for isolation in autophagosomes and successive degradation. In addition, some pharmacological agents, e.g. in-hibitors of mitochondrial ETC and compounds that significantly increase membrane permeability, induce accumulation of ROS and autophagosomes, cause an energy crisis, documented by a de-crease in mitochondrial membrane potential and a fall in ATP content. It is suggested that a fall of ATP level can activate SnRK1, the ortholog of mammalian AMP-dependent proteinkinase (AMPK). This proteinkinase triggers the autophagy by removing the block of negative regulator of autophagy TOR and interaction with autophagic proteins. Interestingly, exogenous treatment of intact wheat roots with natural NO donors such as polyamine spermin induces the formation of autophagosomes without affecting the energy status. In mammals, polyamines induce autophagy due to the depletion of the nucleocytosolic pool of acetyl coenzyme A and the consequent deacetylation of histone proteins before ATP is reduced. This is also mediated by rapid AMPK activation and MTORC1 inactivation. Whether similar mechanism functions in plants is still un-known. In conclusion, the mechanisms that control pro-survival or pro-death functions of autoph-agy in stressed plants depend, among others, on reversibility of the shifts in redox balance and energy metabolism.