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Effect of Mitochondria-Targeted Antioxidant SkQ1 on Programmed Cell Death Induced by Viral Proteins in Tobacco Plants

A. D. Solovieva1, O. Yu. Frolova2, A. G. Solovyev3,4, S. Yu. Morozov3, and A. A. Zamyatnin, Jr.3,5*

1Faculty of Biology, Lomonosov Moscow State University, Leninsky Gory 1/12, 119234 Moscow, Russia; fax: +7 (495) 939-4309

2Institute of Mitoengineering, Lomonosov Moscow State University, Vorobyevy Gory 1/73a, 119992 Moscow, Russia; fax: +7 (495) 939-5945

3Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Leninsky Gory 1/40, 119992 Moscow, Russia; fax: +7 (495) 939-0338

4Institute of Agricultural Biotechnology, Russian Academy of Agricultural Sciences, ul. Timiryazevskaya 42, 127550 Moscow, Russia; fax: +7 (499) 977-0947

5Institute of Molecular Medicine, Sechenov First Moscow State Medical University, ul. Trubetskaya, 8, 119991 Moscow, Russia; fax: +7 (495) 622-9632; E-mail: zamyat@belozersky.msu.ru

* To whom correspondence should be addressed.

Received April 25, 2013
Programmed cell death (PCD) is the main defense mechanism in plants to fight various pathogens including viruses. The best-studied example of virus-induced PCD in plants is Tobacco mosaic virus (TMV)-elicited hypersensitive response in tobacco plants containing the N resistance gene. It was previously reported that the animal mitochondrial protein Bcl-xL, which lacks a homolog in plants, effectively suppresses plant PCD induced by TMV p50 – the elicitor of hypersensitive response in Nicotiana tabacum carrying the N gene. Our studies show that the mitochondria-targeted antioxidant SkQ1 effectively suppresses p50-induced PCD in tobacco plants. On the other hand, SkQ1 did not affect Poa semilatent virus TGB3-induced endoplasmic reticulum stress, which is followed by PCD, in Nicotiana benthamiana epidermal cells. These data suggest that mitochondria-targeted antioxidant SkQ1 can be used to study molecular mechanisms of PCD suppression in plants.
KEY WORDS: mitochondria-targeted compounds, reactive oxygen species, hypersensitive response, ER stress, unfolded protein response

DOI: 10.1134/S000629791309006X