Nitric oxide (NO) as an intermediate in the cryptogein‐induced hypersensitive response – a critical re‐evaluation

ABSTRACT A hypersensitive response (HR) was induced in tobacco leaves and cell suspensions by the fungal elicitor cryptogein, and NO production was followed by chemiluminescence and occasionally by diaminofluorescein (DAF)‐fluorescence. Results from both methods were at least partly consistent, but...

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Veröffentlicht in:Plant, cell and environment cell and environment, 2006-01, Vol.29 (1), p.59-69
Hauptverfasser: PLANCHET, ELISABETH, SONODA, MASATOSHI, ZEIER, JÜRGEN, KAISER, WERNER M.
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SONODA, MASATOSHI
ZEIER, JÜRGEN
KAISER, WERNER M.
description ABSTRACT A hypersensitive response (HR) was induced in tobacco leaves and cell suspensions by the fungal elicitor cryptogein, and NO production was followed by chemiluminescence and occasionally by diaminofluorescein (DAF)‐fluorescence. Results from both methods were at least partly consistent, but kinetics was different. NO emission was not induced by cryptogein in leaves, whereas in cell suspensions some weak NO emission was observed, which was nitrate reductase (NR)‐dependent, but not required for cell death. Nitric oxide synthase (NOS) inhibitors did not prevent cell death, but PR‐1 expression was weakened. In conclusion, neither NR nor NOS appear obligatory for the cryptogein‐induced HR. However, a role for NO was still suggested by the fact that the NO scavenger cPTIO prevented the HR. Unexpectedly, cPTI, the reaction product of cPTIO and NO, also impaired the HR but without scavenging NO. Thus, prevention of the HR by cPTIO is not necessarily indicative for a role of NO. Further, even a 100‐fold NO overproduction (over wild type) by a nitrite reductase‐deficient mutant did not interfere with the cryptogein‐induced HR. Accordingly, the role of NO in the HR should be reconsidered.
doi_str_mv 10.1111/j.1365-3040.2005.01400.x
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Results from both methods were at least partly consistent, but kinetics was different. NO emission was not induced by cryptogein in leaves, whereas in cell suspensions some weak NO emission was observed, which was nitrate reductase (NR)‐dependent, but not required for cell death. Nitric oxide synthase (NOS) inhibitors did not prevent cell death, but PR‐1 expression was weakened. In conclusion, neither NR nor NOS appear obligatory for the cryptogein‐induced HR. However, a role for NO was still suggested by the fact that the NO scavenger cPTIO prevented the HR. Unexpectedly, cPTI, the reaction product of cPTIO and NO, also impaired the HR but without scavenging NO. Thus, prevention of the HR by cPTIO is not necessarily indicative for a role of NO. Further, even a 100‐fold NO overproduction (over wild type) by a nitrite reductase‐deficient mutant did not interfere with the cryptogein‐induced HR. Accordingly, the role of NO in the HR should be reconsidered.</description><identifier>ISSN: 0140-7791</identifier><identifier>EISSN: 1365-3040</identifier><identifier>DOI: 10.1111/j.1365-3040.2005.01400.x</identifier><identifier>PMID: 17086753</identifier><identifier>CODEN: PLCEDV</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Algal Proteins - pharmacology ; Benzoates - pharmacology ; Biological and medical sciences ; Cell Death - drug effects ; chemiluminescence detection ; cryptogein ; Cyclic N-Oxides - pharmacology ; DAF‐2DA ; Fluorescence ; Free Radical Scavengers - metabolism ; Fundamental and applied biological sciences. Psychology ; Fungal Proteins ; Gene Expression Regulation, Plant - drug effects ; Generalities. Disease free stocks ; hypersensitive response ; Imidazoles - pharmacology ; Nicotiana - drug effects ; Nicotiana tabacum ; nitrate reductase ; Nitrate Reductase - metabolism ; nitric oxide ; Nitric Oxide - metabolism ; nitric oxide synthase ; Nitric Oxide Synthase - antagonists &amp; inhibitors ; Phytopathology. Animal pests. 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Results from both methods were at least partly consistent, but kinetics was different. NO emission was not induced by cryptogein in leaves, whereas in cell suspensions some weak NO emission was observed, which was nitrate reductase (NR)‐dependent, but not required for cell death. Nitric oxide synthase (NOS) inhibitors did not prevent cell death, but PR‐1 expression was weakened. In conclusion, neither NR nor NOS appear obligatory for the cryptogein‐induced HR. However, a role for NO was still suggested by the fact that the NO scavenger cPTIO prevented the HR. Unexpectedly, cPTI, the reaction product of cPTIO and NO, also impaired the HR but without scavenging NO. Thus, prevention of the HR by cPTIO is not necessarily indicative for a role of NO. Further, even a 100‐fold NO overproduction (over wild type) by a nitrite reductase‐deficient mutant did not interfere with the cryptogein‐induced HR. Accordingly, the role of NO in the HR should be reconsidered.</description><subject>Algal Proteins - pharmacology</subject><subject>Benzoates - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Death - drug effects</subject><subject>chemiluminescence detection</subject><subject>cryptogein</subject><subject>Cyclic N-Oxides - pharmacology</subject><subject>DAF‐2DA</subject><subject>Fluorescence</subject><subject>Free Radical Scavengers - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fungal Proteins</subject><subject>Gene Expression Regulation, Plant - drug effects</subject><subject>Generalities. Disease free stocks</subject><subject>hypersensitive response</subject><subject>Imidazoles - pharmacology</subject><subject>Nicotiana - drug effects</subject><subject>Nicotiana tabacum</subject><subject>nitrate reductase</subject><subject>Nitrate Reductase - metabolism</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>nitric oxide synthase</subject><subject>Nitric Oxide Synthase - antagonists &amp; inhibitors</subject><subject>Phytopathology. Animal pests. Plant and forest protection</subject><subject>Plant Leaves - drug effects</subject><subject>Plant Proteins - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Time Factors</subject><issn>0140-7791</issn><issn>1365-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQxi0EokvhFZCFBIJDwsR24vjAAa3KH6lqOcDZcpwJ9SrrBDtpd299BCTesE-Cw64AccIXez7_vtFoPkJoAXmRzutNXvCqzDgIyBlAmUMhAPLdPbL6_XGfrBY1k1IVJ-RRjBuAJEj1kJwUEupKlnxFbi7cFJylw861SF9eXL6iJlLjqfMThi22zkyYCjpdIbVhP07DV3T-7va78-1ssaVX-xFDRB_d5K6RBozj4CPSu9sf1CRLkq3pk548eG362Uxu8I_Jg870EZ8c71Py5d3Z5_WH7Pzy_cf12_PMllBCpkprlWoQkaEUrGKlEKxujWmlBQa8wK4C29VcYadE0zWV5VKYJJbKCmz4KXlx6DuG4duMcdJbFy32vfE4zFEzqMtasSKBz_4BN8McfJpNM15BrWSlElQfIBuGGAN2egxua8JeF6CXZPRGLwHoJQC9JKN_JaN3yfr02H9u0lr_GI9RJOD5ETAxLawLxlsX_-KEZIKzxL05cDeux_1_D6A_rc-WF_8Japis6g</recordid><startdate>200601</startdate><enddate>200601</enddate><creator>PLANCHET, ELISABETH</creator><creator>SONODA, MASATOSHI</creator><creator>ZEIER, JÜRGEN</creator><creator>KAISER, WERNER M.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>IQODW</scope><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>7QP</scope><scope>7ST</scope><scope>C1K</scope><scope>SOI</scope><scope>7T7</scope><scope>8FD</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>200601</creationdate><title>Nitric oxide (NO) as an intermediate in the cryptogein‐induced hypersensitive response – a critical re‐evaluation</title><author>PLANCHET, ELISABETH ; SONODA, MASATOSHI ; ZEIER, JÜRGEN ; KAISER, WERNER M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5050-95cc99beee2e7426254428daad7c02031ef60cf839ef94bfb6c374af6059c4eb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Algal Proteins - pharmacology</topic><topic>Benzoates - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Death - drug effects</topic><topic>chemiluminescence detection</topic><topic>cryptogein</topic><topic>Cyclic N-Oxides - pharmacology</topic><topic>DAF‐2DA</topic><topic>Fluorescence</topic><topic>Free Radical Scavengers - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Fungal Proteins</topic><topic>Gene Expression Regulation, Plant - drug effects</topic><topic>Generalities. Disease free stocks</topic><topic>hypersensitive response</topic><topic>Imidazoles - pharmacology</topic><topic>Nicotiana - drug effects</topic><topic>Nicotiana tabacum</topic><topic>nitrate reductase</topic><topic>Nitrate Reductase - metabolism</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>nitric oxide synthase</topic><topic>Nitric Oxide Synthase - antagonists &amp; inhibitors</topic><topic>Phytopathology. Animal pests. Plant and forest protection</topic><topic>Plant Leaves - drug effects</topic><topic>Plant Proteins - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PLANCHET, ELISABETH</creatorcontrib><creatorcontrib>SONODA, MASATOSHI</creatorcontrib><creatorcontrib>ZEIER, JÜRGEN</creatorcontrib><creatorcontrib>KAISER, WERNER M.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Plant, cell and environment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PLANCHET, ELISABETH</au><au>SONODA, MASATOSHI</au><au>ZEIER, JÜRGEN</au><au>KAISER, WERNER M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric oxide (NO) as an intermediate in the cryptogein‐induced hypersensitive response – a critical re‐evaluation</atitle><jtitle>Plant, cell and environment</jtitle><addtitle>Plant Cell Environ</addtitle><date>2006-01</date><risdate>2006</risdate><volume>29</volume><issue>1</issue><spage>59</spage><epage>69</epage><pages>59-69</pages><issn>0140-7791</issn><eissn>1365-3040</eissn><coden>PLCEDV</coden><abstract>ABSTRACT A hypersensitive response (HR) was induced in tobacco leaves and cell suspensions by the fungal elicitor cryptogein, and NO production was followed by chemiluminescence and occasionally by diaminofluorescein (DAF)‐fluorescence. Results from both methods were at least partly consistent, but kinetics was different. NO emission was not induced by cryptogein in leaves, whereas in cell suspensions some weak NO emission was observed, which was nitrate reductase (NR)‐dependent, but not required for cell death. Nitric oxide synthase (NOS) inhibitors did not prevent cell death, but PR‐1 expression was weakened. In conclusion, neither NR nor NOS appear obligatory for the cryptogein‐induced HR. However, a role for NO was still suggested by the fact that the NO scavenger cPTIO prevented the HR. Unexpectedly, cPTI, the reaction product of cPTIO and NO, also impaired the HR but without scavenging NO. Thus, prevention of the HR by cPTIO is not necessarily indicative for a role of NO. Further, even a 100‐fold NO overproduction (over wild type) by a nitrite reductase‐deficient mutant did not interfere with the cryptogein‐induced HR. Accordingly, the role of NO in the HR should be reconsidered.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>17086753</pmid><doi>10.1111/j.1365-3040.2005.01400.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Algal Proteins - pharmacology
Benzoates - pharmacology
Biological and medical sciences
Cell Death - drug effects
chemiluminescence detection
cryptogein
Cyclic N-Oxides - pharmacology
DAF‐2DA
Fluorescence
Free Radical Scavengers - metabolism
Fundamental and applied biological sciences. Psychology
Fungal Proteins
Gene Expression Regulation, Plant - drug effects
Generalities. Disease free stocks
hypersensitive response
Imidazoles - pharmacology
Nicotiana - drug effects
Nicotiana tabacum
nitrate reductase
Nitrate Reductase - metabolism
nitric oxide
Nitric Oxide - metabolism
nitric oxide synthase
Nitric Oxide Synthase - antagonists & inhibitors
Phytopathology. Animal pests. Plant and forest protection
Plant Leaves - drug effects
Plant Proteins - genetics
RNA, Messenger - genetics
RNA, Messenger - metabolism
Time Factors
title Nitric oxide (NO) as an intermediate in the cryptogein‐induced hypersensitive response – a critical re‐evaluation
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