Plant Cell Death Caused by Fungal, Bacterial, and Viral Elicitors: Protective Effect of Mitochondria-Targeted Quinones

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D. B. Kiselevsky¹, O. Yu. Frolova², A. G. Solovyev³, Yu. L. Dorokhov^3,4, S. Yu. Morozov³, and V. D. Samuilov^1*

¹Lomonosov Moscow State University, Faculty of Biology, Leninsky Gory 1-12, 119991 Moscow, Russia; fax: +7 (495) 939-4309; E-mail: vdsamuilov@mail.ru

²Lomonosov Moscow State University, Institute of Mitoengineering, Leninsky Gory 1-75B, 119991 Moscow, Russia; fax: +7 (495) 939-5945

³Lomonosov Moscow State University, Belozersky Institute of Physico-Chemical Biology, Leninsky Gory 1-40, 119991 Moscow, Russia; fax: +7 (495) 939-0338

⁴Vavilov Institute of General Genetics, Russian Academy of Sciences, Gubkina st. 3, 119991 Moscow, Russia; fax: +7 (499) 132-8962

^* To whom correspondence should be addressed.

Received April 27, 2014

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Chitosan (partially deacetylated chitin), a component of fungal cell walls, caused epidermal cell (EC) death in the leaves of pea (Pisum sativum L.) and tobacco Nicotiana tabacum or Nicotiana benthamiana detected by destruction of cell nuclei. The mitochondria-targeted quinone SkQ1 prevented the destruction of EC nuclei induced by chitosan. Chitosan increased and SkQ1 suppressed the activity of protein kinases in N. benthamiana and P. sativum and eliminated the effect of chitosan. Chitosan induced the generation of reactive oxygen species (ROS) in the guard cells (GC) of pea plants. Treatment with chitosan or H₂O₂ did not cause destruction of GC nuclei; however, it resulted in disruption of the permeability barrier of the plasma membrane detected by propidium iodide fluorescence. Treatment with bacterial lipopolysaccharide but not peptidoglycan caused destruction of pea EC nuclei, which was prevented by SkQ1. Leaves of tobacco plants containing the N gene responsible for resistance to tobacco mosaic virus (TMV) were infiltrated with Agrobacterium tumefaciens cells. These cells contained a genetic construct with the gene of the helicase domain of TMV replicase (p50); its protein product p50 is a target for the N-gene product. As a result, the hypersensitive response (HR) was initiated. The HR manifested itself in the death of leaves and was suppressed by SkQ3. Treatment of tobacco epidermal peels with the A. tumefaciens cells for the p50 gene expression stimulated the destruction of EC nuclei, which was inhibited by SkQ1 or SkQ3. The p50-lacking A. tumefaciens cells did not induce the destruction of EC nuclei. The protective effect of mitochondria-targeted antioxidants SkQ1 and SkQ3 demonstrates the involvement of mitochondria and their ROS in programmed cell death caused by pathogen elicitors.

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KEY WORDS: programmed cell death, mitochondria-targeted quinones, chitosan, lipopolysaccharide, peptidoglycan, tobacco mosaic virus, guard cells, epidermal cells

DOI: 10.1134/S0006297914120050

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