Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones
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 de...
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| Veröffentlicht in: | Biochemistry (Moscow) 2014-12, Vol.79 (12), p.1322-1332 |
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| creator | Kiselevsky, D. B. Frolova, O. Yu Solovyev, A. G. Dorokhov, Yu. L. Morozov, S. Yu Samuilov, V. D. |
| description | 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 H
2
O
2
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. |
| doi_str_mv | 10.1134/S0006297914120050 |
| format | Article |
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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 H
2
O
2
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.</description><identifier>ISSN: 0006-2979</identifier><identifier>EISSN: 1608-3040</identifier><identifier>DOI: 10.1134/S0006297914120050</identifier><identifier>PMID: 25716725</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Agrobacterium tumefaciens ; Antioxidants ; Antioxidants - pharmacology ; Bacteria ; Bacterial Physiological Phenomena ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Bioorganic Chemistry ; Botanical research ; Cell death ; Cell Death - drug effects ; Cell Nucleus - drug effects ; Cell Nucleus - metabolism ; Cell research ; Cellular biology ; Chitin ; Flowers & plants ; Fungi - physiology ; Health aspects ; Hydrogen peroxide ; Iodides ; Leaves ; Life Sciences ; Microbiology ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mortality ; Nicotiana - cytology ; Nicotiana - drug effects ; Nicotiana - microbiology ; Nicotiana - virology ; Nicotiana benthamiana ; Nicotiana tabacum ; Pathogens ; Pisum sativum ; Pisum sativum - cytology ; Pisum sativum - drug effects ; Pisum sativum - microbiology ; Pisum sativum - virology ; Plant cells and tissues ; Plant mitochondria ; Plant-pathogen relationships ; Plastoquinone - analogs & derivatives ; Plastoquinone - pharmacology ; Quinone ; Tobacco ; Tobacco mosaic virus ; Tobacco Mosaic Virus - physiology</subject><ispartof>Biochemistry (Moscow), 2014-12, Vol.79 (12), p.1322-1332</ispartof><rights>Pleiades Publishing, Ltd. 2014</rights><rights>COPYRIGHT 2014 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-bc31291944ac761b228d5226167c4c803a7c5482e798a8d1da635de8fb36a9053</citedby><cites>FETCH-LOGICAL-c472t-bc31291944ac761b228d5226167c4c803a7c5482e798a8d1da635de8fb36a9053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0006297914120050$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0006297914120050$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25716725$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kiselevsky, D. B.</creatorcontrib><creatorcontrib>Frolova, O. Yu</creatorcontrib><creatorcontrib>Solovyev, A. G.</creatorcontrib><creatorcontrib>Dorokhov, Yu. L.</creatorcontrib><creatorcontrib>Morozov, S. Yu</creatorcontrib><creatorcontrib>Samuilov, V. D.</creatorcontrib><title>Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones</title><title>Biochemistry (Moscow)</title><addtitle>Biochemistry Moscow</addtitle><addtitle>Biochemistry (Mosc)</addtitle><description>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 H
2
O
2
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.</description><subject>Agrobacterium tumefaciens</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Bacteria</subject><subject>Bacterial Physiological Phenomena</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bioorganic Chemistry</subject><subject>Botanical research</subject><subject>Cell death</subject><subject>Cell Death - drug effects</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Cell research</subject><subject>Cellular biology</subject><subject>Chitin</subject><subject>Flowers & plants</subject><subject>Fungi - physiology</subject><subject>Health aspects</subject><subject>Hydrogen peroxide</subject><subject>Iodides</subject><subject>Leaves</subject><subject>Life Sciences</subject><subject>Microbiology</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mortality</subject><subject>Nicotiana - cytology</subject><subject>Nicotiana - drug effects</subject><subject>Nicotiana - microbiology</subject><subject>Nicotiana - virology</subject><subject>Nicotiana benthamiana</subject><subject>Nicotiana tabacum</subject><subject>Pathogens</subject><subject>Pisum sativum</subject><subject>Pisum sativum - cytology</subject><subject>Pisum sativum - drug effects</subject><subject>Pisum sativum - microbiology</subject><subject>Pisum sativum - virology</subject><subject>Plant cells and tissues</subject><subject>Plant mitochondria</subject><subject>Plant-pathogen relationships</subject><subject>Plastoquinone - analogs & derivatives</subject><subject>Plastoquinone - pharmacology</subject><subject>Quinone</subject><subject>Tobacco</subject><subject>Tobacco mosaic virus</subject><subject>Tobacco Mosaic Virus - physiology</subject><issn>0006-2979</issn><issn>1608-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkl1rFTEQhoMo9lj9Ad5IwJteuDVfm2y8K8UvKCio10s2mT1N2ZNtk-yB_ntnOfVbQULIJPO8LzNhCHnK2SnnUr38xBjTwhrLFReMtewe2XDNukYyxe6TzZpu1vwReVTKFV4Fs_IhORKt4dqIdkP2HyeXKvUwTTSAq5fUu6VAoMMtHZe0ddMLOjhfIcc1dCnQfcxuojBFH-ucyyt6necKvsY9UBhHjOg80h0m_eWcAgqb6vIWKrreLDHNCcpj8mB0U4End-cx-fLm9efzd83Fh7fvz88uGq-MqM3gJReWW6WcN5oPQnShFUJj8V75jklnfKs6AcZ2rgs8OC3bAN04SO0sa-UxOTn4Yo03C5Ta72JZm3UJ5qX0XLfW4Jbqf1ClDTfKIvr8N_RqXnLCRpCSLdfWdPwHhZ8IfUzjXLPzq2l_Jq3mstNCI3X6FwpXgF30-FdjxPdfBPwg8HkuJcPYX-e4c_m256xfx6L_YyxQ8-yu4GXYQfiu-DYHCIgDUDCVtpB_6uifrl8BR_K-rA</recordid><startdate>20141201</startdate><enddate>20141201</enddate><creator>Kiselevsky, D. B.</creator><creator>Frolova, O. Yu</creator><creator>Solovyev, A. G.</creator><creator>Dorokhov, Yu. L.</creator><creator>Morozov, S. Yu</creator><creator>Samuilov, V. D.</creator><general>Pleiades Publishing</general><general>Springer</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7T7</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20141201</creationdate><title>Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones</title><author>Kiselevsky, D. B. ; Frolova, O. Yu ; Solovyev, A. G. ; Dorokhov, Yu. L. ; Morozov, S. Yu ; Samuilov, V. D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-bc31291944ac761b228d5226167c4c803a7c5482e798a8d1da635de8fb36a9053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Agrobacterium tumefaciens</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Bacteria</topic><topic>Bacterial Physiological Phenomena</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bioorganic Chemistry</topic><topic>Botanical research</topic><topic>Cell death</topic><topic>Cell Death - drug effects</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Cell research</topic><topic>Cellular biology</topic><topic>Chitin</topic><topic>Flowers & plants</topic><topic>Fungi - physiology</topic><topic>Health aspects</topic><topic>Hydrogen peroxide</topic><topic>Iodides</topic><topic>Leaves</topic><topic>Life Sciences</topic><topic>Microbiology</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mortality</topic><topic>Nicotiana - cytology</topic><topic>Nicotiana - drug effects</topic><topic>Nicotiana - microbiology</topic><topic>Nicotiana - virology</topic><topic>Nicotiana benthamiana</topic><topic>Nicotiana tabacum</topic><topic>Pathogens</topic><topic>Pisum sativum</topic><topic>Pisum sativum - cytology</topic><topic>Pisum sativum - drug effects</topic><topic>Pisum sativum - microbiology</topic><topic>Pisum sativum - virology</topic><topic>Plant cells and tissues</topic><topic>Plant mitochondria</topic><topic>Plant-pathogen relationships</topic><topic>Plastoquinone - analogs & derivatives</topic><topic>Plastoquinone - pharmacology</topic><topic>Quinone</topic><topic>Tobacco</topic><topic>Tobacco mosaic virus</topic><topic>Tobacco Mosaic Virus - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kiselevsky, D. B.</creatorcontrib><creatorcontrib>Frolova, O. Yu</creatorcontrib><creatorcontrib>Solovyev, A. G.</creatorcontrib><creatorcontrib>Dorokhov, Yu. L.</creatorcontrib><creatorcontrib>Morozov, S. Yu</creatorcontrib><creatorcontrib>Samuilov, V. D.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemistry (Moscow)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kiselevsky, D. B.</au><au>Frolova, O. Yu</au><au>Solovyev, A. G.</au><au>Dorokhov, Yu. L.</au><au>Morozov, S. Yu</au><au>Samuilov, V. D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones</atitle><jtitle>Biochemistry (Moscow)</jtitle><stitle>Biochemistry Moscow</stitle><addtitle>Biochemistry (Mosc)</addtitle><date>2014-12-01</date><risdate>2014</risdate><volume>79</volume><issue>12</issue><spage>1322</spage><epage>1332</epage><pages>1322-1332</pages><issn>0006-2979</issn><eissn>1608-3040</eissn><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 H
2
O
2
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.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><pmid>25716725</pmid><doi>10.1134/S0006297914120050</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-2979 |
| ispartof | Biochemistry (Moscow), 2014-12, Vol.79 (12), p.1322-1332 |
| issn | 0006-2979 1608-3040 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1659765934 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Agrobacterium tumefaciens Antioxidants Antioxidants - pharmacology Bacteria Bacterial Physiological Phenomena Biochemistry Biomedical and Life Sciences Biomedicine Bioorganic Chemistry Botanical research Cell death Cell Death - drug effects Cell Nucleus - drug effects Cell Nucleus - metabolism Cell research Cellular biology Chitin Flowers & plants Fungi - physiology Health aspects Hydrogen peroxide Iodides Leaves Life Sciences Microbiology Mitochondria - drug effects Mitochondria - metabolism Mortality Nicotiana - cytology Nicotiana - drug effects Nicotiana - microbiology Nicotiana - virology Nicotiana benthamiana Nicotiana tabacum Pathogens Pisum sativum Pisum sativum - cytology Pisum sativum - drug effects Pisum sativum - microbiology Pisum sativum - virology Plant cells and tissues Plant mitochondria Plant-pathogen relationships Plastoquinone - analogs & derivatives Plastoquinone - pharmacology Quinone Tobacco Tobacco mosaic virus Tobacco Mosaic Virus - physiology |
| title | Plant cell death caused by fungal, bacterial, and viral elicitors: protective effect of mitochondria-targeted quinones |
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