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

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A. D. Solovieva¹, O. Yu. Frolova², A. G. Solovyev^3,4, 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

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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.

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KEY WORDS: mitochondria-targeted compounds, reactive oxygen species, hypersensitive response, ER stress, unfolded protein response

DOI: 10.1134/S000629791309006X

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