NO signalling in cytokinin-induced programmed cell death
Cell death can be induced by cytokinin 6-benzylaminopurine (BA) at high dosage in suspension-cultured Arabidopsis cells. Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented wi...
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| Veröffentlicht in: | Plant, cell and environment cell and environment, 2005-09, Vol.28 (9), p.1171-1178 |
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| container_title | Plant, cell and environment |
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| creator | Carimi, F Zottini, M Costa, A Cattelan, I De Michele, R Terzi, M Lo Schiavo, F |
| description | Cell death can be induced by cytokinin 6-benzylaminopurine (BA) at high dosage in suspension-cultured Arabidopsis cells. Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or the nitric oxide synthase (NOS) inhibitors: 2-aminoethyl-isothiourea (AET) and N(G.)-monomethyl-L-arginine (L-NMMA), which suggests that NO is produced via a NOS and is a signalling component of this form of programmed cell death. In BA-treated cells, mitochondrial functionality is altered via inhibition of respiration. This inhibition can be prevented by addition of either cPTIO or AET implying that NO acts at the mitochondrial level. |
| doi_str_mv | 10.1111/j.1365-3040.2005.01355.x |
| format | Article |
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Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or the nitric oxide synthase (NOS) inhibitors: 2-aminoethyl-isothiourea (AET) and N(G.)-monomethyl-L-arginine (L-NMMA), which suggests that NO is produced via a NOS and is a signalling component of this form of programmed cell death. In BA-treated cells, mitochondrial functionality is altered via inhibition of respiration. This inhibition can be prevented by addition of either cPTIO or AET implying that NO acts at the mitochondrial level.</description><identifier>ISSN: 0140-7791</identifier><identifier>EISSN: 1365-3040</identifier><identifier>DOI: 10.1111/j.1365-3040.2005.01355.x</identifier><identifier>CODEN: PLCEDV</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>apoptosis ; Arabidopsis ; Arabidopsis thaliana ; benzyladenine ; Biological and medical sciences ; biosynthesis ; Cell death ; Cell physiology ; cell respiration ; cell suspension culture ; cultured cells ; cytokinins ; Fundamental and applied biological sciences. Psychology ; mitochondria ; Molecular and cellular biology ; nitric oxide ; nitric oxide synthase ; programmed cell death ; senescence ; Signal transduction</subject><ispartof>Plant, cell and environment, 2005-09, Vol.28 (9), p.1171-1178</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Sep 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4445-f565ea027fcf64916af7bcde3d4031bfab01284d1d51bc81c3c28d07ef15c20c3</citedby><cites>FETCH-LOGICAL-c4445-f565ea027fcf64916af7bcde3d4031bfab01284d1d51bc81c3c28d07ef15c20c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-3040.2005.01355.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-3040.2005.01355.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,1428,27905,27906,45555,45556,46390,46814</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17050795$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Carimi, F</creatorcontrib><creatorcontrib>Zottini, M</creatorcontrib><creatorcontrib>Costa, A</creatorcontrib><creatorcontrib>Cattelan, I</creatorcontrib><creatorcontrib>De Michele, R</creatorcontrib><creatorcontrib>Terzi, M</creatorcontrib><creatorcontrib>Lo Schiavo, F</creatorcontrib><title>NO signalling in cytokinin-induced programmed cell death</title><title>Plant, cell and environment</title><description>Cell death can be induced by cytokinin 6-benzylaminopurine (BA) at high dosage in suspension-cultured Arabidopsis cells. Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or the nitric oxide synthase (NOS) inhibitors: 2-aminoethyl-isothiourea (AET) and N(G.)-monomethyl-L-arginine (L-NMMA), which suggests that NO is produced via a NOS and is a signalling component of this form of programmed cell death. In BA-treated cells, mitochondrial functionality is altered via inhibition of respiration. This inhibition can be prevented by addition of either cPTIO or AET implying that NO acts at the mitochondrial level.</description><subject>apoptosis</subject><subject>Arabidopsis</subject><subject>Arabidopsis thaliana</subject><subject>benzyladenine</subject><subject>Biological and medical sciences</subject><subject>biosynthesis</subject><subject>Cell death</subject><subject>Cell physiology</subject><subject>cell respiration</subject><subject>cell suspension culture</subject><subject>cultured cells</subject><subject>cytokinins</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>mitochondria</subject><subject>Molecular and cellular biology</subject><subject>nitric oxide</subject><subject>nitric oxide synthase</subject><subject>programmed cell death</subject><subject>senescence</subject><subject>Signal transduction</subject><issn>0140-7791</issn><issn>1365-3040</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNqNkMtOwzAQRS0EEuXxDURILBNm_IjTBQtUlYdUUSRgbbmOXVzSBOxWtH-PQxFsmc2M7HvvjA4hGUKBqS4XBbJS5Aw4FBRAFIBMiGKzRwa_H_tkAMghl3KIh-QoxgVAepDDAakepln081Y3jW_nmW8zs111b771be7bem1snb2Hbh70cplGY5smq61evZ6QA6ebaE9_-jF5uRk_j-7yyfT2fnQ9yQ3nXOROlMJqoNIZV_IhltrJmaktqzkwnDk9A6QVr7EWODMVGmZoVYO0DoWhYNgxOd_lpis-1jau1KJbh3RvVJSVUFHkmETVTmRCF2OwTr0Hv9RhqxBUj0ktVE9D9TRUj0l9Y1KbZL34ydfR6MYF3Rof__wSBMihSLqrne7TN3b773z1OBr3U_Kf7fxOd0rPQ9rx8kSTChAoL1GyL20jgu8</recordid><startdate>200509</startdate><enddate>200509</enddate><creator>Carimi, F</creator><creator>Zottini, M</creator><creator>Costa, A</creator><creator>Cattelan, I</creator><creator>De Michele, R</creator><creator>Terzi, M</creator><creator>Lo Schiavo, F</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Wiley Subscription Services, Inc</general><scope>FBQ</scope><scope>IQODW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7ST</scope><scope>C1K</scope><scope>SOI</scope></search><sort><creationdate>200509</creationdate><title>NO signalling in cytokinin-induced programmed cell death</title><author>Carimi, F ; Zottini, M ; Costa, A ; Cattelan, I ; De Michele, R ; Terzi, M ; Lo Schiavo, F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4445-f565ea027fcf64916af7bcde3d4031bfab01284d1d51bc81c3c28d07ef15c20c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>apoptosis</topic><topic>Arabidopsis</topic><topic>Arabidopsis thaliana</topic><topic>benzyladenine</topic><topic>Biological and medical sciences</topic><topic>biosynthesis</topic><topic>Cell death</topic><topic>Cell physiology</topic><topic>cell respiration</topic><topic>cell suspension culture</topic><topic>cultured cells</topic><topic>cytokinins</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>mitochondria</topic><topic>Molecular and cellular biology</topic><topic>nitric oxide</topic><topic>nitric oxide synthase</topic><topic>programmed cell death</topic><topic>senescence</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Carimi, F</creatorcontrib><creatorcontrib>Zottini, M</creatorcontrib><creatorcontrib>Costa, A</creatorcontrib><creatorcontrib>Cattelan, I</creatorcontrib><creatorcontrib>De Michele, R</creatorcontrib><creatorcontrib>Terzi, M</creatorcontrib><creatorcontrib>Lo Schiavo, F</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><jtitle>Plant, cell and environment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Carimi, F</au><au>Zottini, M</au><au>Costa, A</au><au>Cattelan, I</au><au>De Michele, R</au><au>Terzi, M</au><au>Lo Schiavo, F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>NO signalling in cytokinin-induced programmed cell death</atitle><jtitle>Plant, cell and environment</jtitle><date>2005-09</date><risdate>2005</risdate><volume>28</volume><issue>9</issue><spage>1171</spage><epage>1178</epage><pages>1171-1178</pages><issn>0140-7791</issn><eissn>1365-3040</eissn><coden>PLCEDV</coden><abstract>Cell death can be induced by cytokinin 6-benzylaminopurine (BA) at high dosage in suspension-cultured Arabidopsis cells. Herein, we provide evidence that BA induces nitric oxide (NO) synthesis in a dose-dependent manner. A reduction in cell death can be observed when the cytokinin is supplemented with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) or the nitric oxide synthase (NOS) inhibitors: 2-aminoethyl-isothiourea (AET) and N(G.)-monomethyl-L-arginine (L-NMMA), which suggests that NO is produced via a NOS and is a signalling component of this form of programmed cell death. In BA-treated cells, mitochondrial functionality is altered via inhibition of respiration. This inhibition can be prevented by addition of either cPTIO or AET implying that NO acts at the mitochondrial level.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><doi>10.1111/j.1365-3040.2005.01355.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | apoptosis Arabidopsis Arabidopsis thaliana benzyladenine Biological and medical sciences biosynthesis Cell death Cell physiology cell respiration cell suspension culture cultured cells cytokinins Fundamental and applied biological sciences. Psychology mitochondria Molecular and cellular biology nitric oxide nitric oxide synthase programmed cell death senescence Signal transduction |
| title | NO signalling in cytokinin-induced programmed cell death |
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