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Funct Plant Biol. 2018 Jan;45(2):247-258. doi: 10.1071/FP16418.

The levels of peroxisomal catalase protein and activity modulate the onset of cell death in tobacco BY-2 cells via reactive oxygen species levels and autophagy.

Functional plant biology : FPB

Elena V Tyutereva, Ksenia S Dobryakova, Andreas Schiermeyer, Maria F Shishova, Katharina Pawlowski, Vadim Demidchik, Sigrun Reumann, Olga V Voitsekhovskaja

Affiliations

  1. Laboratory of Molecular and Ecological Physiology, Komarov Botanical Institute, Russian Academy of Sciences, ul. Professora Popova 2, 197376 Saint Petersburg, Russia.
  2. Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Department of Plant Biotechnology, Forckenbeckstrasse 6, D-52074 Aachen, Germany.
  3. Department of Physiology and Biochemistry of Plants, Saint Petersburg State University, Universitetskaya em., 7/9, 199034 Saint Petersburg, Russia.
  4. Department of Ecology, Environment and Plant Sciences, Stockholm University, 106 91 Stockholm, Sweden.
  5. Department of Plant Biochemistry, Albrecht-von-Haller-Institute for Plant Sciences, Georg-August-University of Goettingen, Justus-von-Liebig Weg 11, D-37077, Goettingen, Germany.

PMID: 32291039 DOI: 10.1071/FP16418

Abstract

In plant cells, peroxisomes participate in the metabolism of reactive oxygen species (ROS). One of the major regulators of cellular ROS levels - catalase (CAT) - occurs exclusively in peroxisomes. CAT activity is required for immunity-triggered autophagic programmed cell death (PCD). Autophagy has been recently demonstrated to represent a route for degradation of peroxisomes in plant cells. In the present study, the dynamics of the cellular peroxisome pool in tobacco BY-2 cell suspension cultures were used to analyse the effects of inhibition of basal autophagy with special attention to CAT activity. Numbers of peroxisomes per cell, levels of CAT protein and activity, cell viability, ROS levels and expression levels of genes encoding components of antioxidant system were analysed upon application of 3-methyladenine (3-MA), an inhibitor of autophagy, and/or aminotriazole (AT), an inhibitor of CAT. When applied separately, 3-MA and AT led to an increase in cell death, but this effect was attenuated by their simultaneous application. The obtained data suggest that both the levels of CAT protein in peroxisomes as well as CAT activity modulate the onset of cell death in tobacco BY-2 cells via ROS levels and autophagy.

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