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: email@example.com
* 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