NDLI: Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones

Content Provider	Springer Nature Link
Author	Kiselevsky, D. B. Frolova, O. Yu. Solovyev, A. G. Dorokhov, Yu. L. Morozov, S. Yu. Samuilov, V. D.
Copyright Year	2014
Abstract	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.
Starting Page	1322
Ending Page	1332
Page Count	11
File Format	PDF
ISSN	00062979
Journal	Biochemistry (Moscow)
Volume Number	79
Issue Number	12
e-ISSN	16083040
Language	English
Publisher	Pleiades Publishing
Publisher Date	2014-12-13
Publisher Place	Moscow
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	programmed cell death mitochondria-targeted quinones chitosan lipopolysaccharide peptidoglycan tobacco mosaic virus guard cells epidermal cells Biochemistry Bioorganic Chemistry Microbiology Biomedicine general
Content Type	Text
Resource Type	Article
Subject	Biochemistry Biophysics Geriatrics and Gerontology

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