Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus
The hypersensitive response (HR) of disease-resistant plant cells to fungal invasion is a rapid cell death that has some features in common with programmed cell death (apoptosis) in animals. We investigated the role of cytosolic free calcium ([Ca2+]i) in the HR of cowpea to the cowpea rust fungus. B...
Gespeichert in:
Veröffentlicht in: | The Plant cell 1998-04, Vol.10 (4), p.585-597 |
---|---|
Hauptverfasser: | , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 597 |
---|---|
container_issue | 4 |
container_start_page | 585 |
container_title | The Plant cell |
container_volume | 10 |
creator | Xu, H. (University of Toronto, Ontario, Canada.) Heath, M.C |
description | The hypersensitive response (HR) of disease-resistant plant cells to fungal invasion is a rapid cell death that has some features in common with programmed cell death (apoptosis) in animals. We investigated the role of cytosolic free calcium ([Ca2+]i) in the HR of cowpea to the cowpea rust fungus. By using confocal laser scanning microscopy in conjunction with a calcium reporter dye, we found a slow, prolonged elevation of [Ca2+]i in epidermal cells of resistant but not susceptible plants as the fungus grew through the cell wall. [Ca2+]i levels declined to normal levels as the fungus entered and grew within the cell lumen. This elevation was related to the stage of fungal growth and not to the speed of initiation of subsequent cell death. Elevated [Ca2+]i levels also represent the first sign of the HR detectable in this cowpea-cowpea rust fungus system. The increase in [Ca2+]i was prevented by calcium channel inhibitors. This effect was consistent with pharmacological tests in which these inhibitors delayed the HR. The data suggest that elevation of [Ca2+]i is involved in signal transduction leading to the HR during rust fungal infection |
doi_str_mv | 10.1105/tpc.10.4.585 |
format | Article |
fullrecord | <record><control><sourceid>jstor_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_144015</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>3870734</jstor_id><sourcerecordid>3870734</sourcerecordid><originalsourceid>FETCH-LOGICAL-c560t-cc133ebc07bf846cbddfaa1c11efe67d10663545b338328ee14fc38b0eb02cb13</originalsourceid><addsrcrecordid>eNp9kc2OFCEURonRjGPrzq0JC2NcWC0UUEUtZmEm_iWTmKiTuCMUXLqZVEMJxZh-Bx9aOt0Zx40rbriHw4UPoeeUrCkl4u0ym3Wt-VpI8QCdU8Haph3kj4e1Jpw0vBP0MXqS8w0hhPZ0OENng-BykPwc_f4aJ8DRYaMn48sO-4Cz3wQ94SXpkG0xi48B25J82OBlC3i7nyFlCNkv_hZwgjzHkKEaSgaLxz0edfbWx7qfoLGQKmar2MHRVW87eEz8NYPGqeQFuxI2JT9Fj5yeMjw7rSt0_eH998tPzdWXj58v3101RnRkaYyhjMFoSD86yTszWuu0poZScND1lpKuY4KLkTHJWglAuTNMjgRG0pqRshW6OHrnMu7AGgj1rZOak9_ptFdRe_VvJ_it2sRbRTkn9X9X6PXpfIo_C-RF7Xw2ME06QCxZUSkG2nay7Sr66v9oL_pWDLKCb46gSTHnBO5uHErUIWdVcz7UXNWcK_7i_hPu4FOwtf_y2L_JS0z3XS0jvWKyJz3jfzVOR6U3yWd1_Y0OQ0-GOrxgfwA5Ar2q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17572598</pqid></control><display><type>article</type><title>Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>JSTOR Archive Collection A-Z Listing</source><source>Oxford University Press Journals All Titles (1996-Current)</source><creator>Xu, H. (University of Toronto, Ontario, Canada.) ; Heath, M.C</creator><creatorcontrib>Xu, H. (University of Toronto, Ontario, Canada.) ; Heath, M.C</creatorcontrib><description>The hypersensitive response (HR) of disease-resistant plant cells to fungal invasion is a rapid cell death that has some features in common with programmed cell death (apoptosis) in animals. We investigated the role of cytosolic free calcium ([Ca2+]i) in the HR of cowpea to the cowpea rust fungus. By using confocal laser scanning microscopy in conjunction with a calcium reporter dye, we found a slow, prolonged elevation of [Ca2+]i in epidermal cells of resistant but not susceptible plants as the fungus grew through the cell wall. [Ca2+]i levels declined to normal levels as the fungus entered and grew within the cell lumen. This elevation was related to the stage of fungal growth and not to the speed of initiation of subsequent cell death. Elevated [Ca2+]i levels also represent the first sign of the HR detectable in this cowpea-cowpea rust fungus system. The increase in [Ca2+]i was prevented by calcium channel inhibitors. This effect was consistent with pharmacological tests in which these inhibitors delayed the HR. The data suggest that elevation of [Ca2+]i is involved in signal transduction leading to the HR during rust fungal infection</description><identifier>ISSN: 1040-4651</identifier><identifier>EISSN: 1532-298X</identifier><identifier>DOI: 10.1105/tpc.10.4.585</identifier><identifier>PMID: 9548984</identifier><language>eng</language><publisher>United States: American Society of Plant Physiologists</publisher><subject>ANTIMETABOLITE ; ANTIMETABOLITES ; ANTIMETABOLITOS ; BIOCHEMISTRY ; BIOCHIMIE ; BIOQUIMICA ; CALCIO ; CALCIUM ; CALCIUM CHANNEL INHIBITORS ; CARDIOVASCULAR AGENTS ; CATION ; CATIONES ; CATIONS ; Cell death ; Cell nucleus ; CELL WALLS ; CYTOCHEMISTRY ; DEFENCE MECHANISMS ; DISEASE RESISTANCE ; Dyes ; EGTA ; ELEMENTOS DE TIERRAS RARAS ; Epidermal cells ; EPIDERME ; EPIDERMIS ; ESPORAS FUNGICAS ; FUNGAL SPORES ; Fungi ; HYPHAE ; INFECCION ; INFECTION ; KINETIN ; KINETINE ; LANTHANUM ; LANTHANUM CHLORIDE ; MECANISME DE DEFENSE ; MECANISMOS DE DEFENSA ; MEDICAMENTOS CARDIOVASCULARES ; METAL DES TERRES RARES ; MICELIO ; MODIFICATEUR CARDIOVASCULAIRE ; MYCELIUM ; PARED CELULAR ; PAROI CELLULAIRE ; Plant cells ; Plants ; QUINETINA ; RARE EARTH ELEMENTS ; Ratio analysis ; RESISTANCE AUX MALADIES ; RESISTENCIA A LA ENFERMEDAD ; ROUILLE ; ROYA ; RUSTS ; SPORE FONGIQUE ; TMB-8 ; UROMYCES APPENDICULATUS ; VERAPAMIL ; VIGNA UNGUICULATA</subject><ispartof>The Plant cell, 1998-04, Vol.10 (4), p.585-597</ispartof><rights>Copyright 1998 American Society of Plant Physiologists</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c560t-cc133ebc07bf846cbddfaa1c11efe67d10663545b338328ee14fc38b0eb02cb13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3870734$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3870734$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,315,781,785,804,886,27929,27930,58022,58255</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9548984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, H. (University of Toronto, Ontario, Canada.)</creatorcontrib><creatorcontrib>Heath, M.C</creatorcontrib><title>Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus</title><title>The Plant cell</title><addtitle>Plant Cell</addtitle><description>The hypersensitive response (HR) of disease-resistant plant cells to fungal invasion is a rapid cell death that has some features in common with programmed cell death (apoptosis) in animals. We investigated the role of cytosolic free calcium ([Ca2+]i) in the HR of cowpea to the cowpea rust fungus. By using confocal laser scanning microscopy in conjunction with a calcium reporter dye, we found a slow, prolonged elevation of [Ca2+]i in epidermal cells of resistant but not susceptible plants as the fungus grew through the cell wall. [Ca2+]i levels declined to normal levels as the fungus entered and grew within the cell lumen. This elevation was related to the stage of fungal growth and not to the speed of initiation of subsequent cell death. Elevated [Ca2+]i levels also represent the first sign of the HR detectable in this cowpea-cowpea rust fungus system. The increase in [Ca2+]i was prevented by calcium channel inhibitors. This effect was consistent with pharmacological tests in which these inhibitors delayed the HR. The data suggest that elevation of [Ca2+]i is involved in signal transduction leading to the HR during rust fungal infection</description><subject>ANTIMETABOLITE</subject><subject>ANTIMETABOLITES</subject><subject>ANTIMETABOLITOS</subject><subject>BIOCHEMISTRY</subject><subject>BIOCHIMIE</subject><subject>BIOQUIMICA</subject><subject>CALCIO</subject><subject>CALCIUM</subject><subject>CALCIUM CHANNEL INHIBITORS</subject><subject>CARDIOVASCULAR AGENTS</subject><subject>CATION</subject><subject>CATIONES</subject><subject>CATIONS</subject><subject>Cell death</subject><subject>Cell nucleus</subject><subject>CELL WALLS</subject><subject>CYTOCHEMISTRY</subject><subject>DEFENCE MECHANISMS</subject><subject>DISEASE RESISTANCE</subject><subject>Dyes</subject><subject>EGTA</subject><subject>ELEMENTOS DE TIERRAS RARAS</subject><subject>Epidermal cells</subject><subject>EPIDERME</subject><subject>EPIDERMIS</subject><subject>ESPORAS FUNGICAS</subject><subject>FUNGAL SPORES</subject><subject>Fungi</subject><subject>HYPHAE</subject><subject>INFECCION</subject><subject>INFECTION</subject><subject>KINETIN</subject><subject>KINETINE</subject><subject>LANTHANUM</subject><subject>LANTHANUM CHLORIDE</subject><subject>MECANISME DE DEFENSE</subject><subject>MECANISMOS DE DEFENSA</subject><subject>MEDICAMENTOS CARDIOVASCULARES</subject><subject>METAL DES TERRES RARES</subject><subject>MICELIO</subject><subject>MODIFICATEUR CARDIOVASCULAIRE</subject><subject>MYCELIUM</subject><subject>PARED CELULAR</subject><subject>PAROI CELLULAIRE</subject><subject>Plant cells</subject><subject>Plants</subject><subject>QUINETINA</subject><subject>RARE EARTH ELEMENTS</subject><subject>Ratio analysis</subject><subject>RESISTANCE AUX MALADIES</subject><subject>RESISTENCIA A LA ENFERMEDAD</subject><subject>ROUILLE</subject><subject>ROYA</subject><subject>RUSTS</subject><subject>SPORE FONGIQUE</subject><subject>TMB-8</subject><subject>UROMYCES APPENDICULATUS</subject><subject>VERAPAMIL</subject><subject>VIGNA UNGUICULATA</subject><issn>1040-4651</issn><issn>1532-298X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNp9kc2OFCEURonRjGPrzq0JC2NcWC0UUEUtZmEm_iWTmKiTuCMUXLqZVEMJxZh-Bx9aOt0Zx40rbriHw4UPoeeUrCkl4u0ym3Wt-VpI8QCdU8Haph3kj4e1Jpw0vBP0MXqS8w0hhPZ0OENng-BykPwc_f4aJ8DRYaMn48sO-4Cz3wQ94SXpkG0xi48B25J82OBlC3i7nyFlCNkv_hZwgjzHkKEaSgaLxz0edfbWx7qfoLGQKmar2MHRVW87eEz8NYPGqeQFuxI2JT9Fj5yeMjw7rSt0_eH998tPzdWXj58v3101RnRkaYyhjMFoSD86yTszWuu0poZScND1lpKuY4KLkTHJWglAuTNMjgRG0pqRshW6OHrnMu7AGgj1rZOak9_ptFdRe_VvJ_it2sRbRTkn9X9X6PXpfIo_C-RF7Xw2ME06QCxZUSkG2nay7Sr66v9oL_pWDLKCb46gSTHnBO5uHErUIWdVcz7UXNWcK_7i_hPu4FOwtf_y2L_JS0z3XS0jvWKyJz3jfzVOR6U3yWd1_Y0OQ0-GOrxgfwA5Ar2q</recordid><startdate>19980401</startdate><enddate>19980401</enddate><creator>Xu, H. (University of Toronto, Ontario, Canada.)</creator><creator>Heath, M.C</creator><general>American Society of Plant Physiologists</general><scope>FBQ</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19980401</creationdate><title>Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus</title><author>Xu, H. (University of Toronto, Ontario, Canada.) ; Heath, M.C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c560t-cc133ebc07bf846cbddfaa1c11efe67d10663545b338328ee14fc38b0eb02cb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>ANTIMETABOLITE</topic><topic>ANTIMETABOLITES</topic><topic>ANTIMETABOLITOS</topic><topic>BIOCHEMISTRY</topic><topic>BIOCHIMIE</topic><topic>BIOQUIMICA</topic><topic>CALCIO</topic><topic>CALCIUM</topic><topic>CALCIUM CHANNEL INHIBITORS</topic><topic>CARDIOVASCULAR AGENTS</topic><topic>CATION</topic><topic>CATIONES</topic><topic>CATIONS</topic><topic>Cell death</topic><topic>Cell nucleus</topic><topic>CELL WALLS</topic><topic>CYTOCHEMISTRY</topic><topic>DEFENCE MECHANISMS</topic><topic>DISEASE RESISTANCE</topic><topic>Dyes</topic><topic>EGTA</topic><topic>ELEMENTOS DE TIERRAS RARAS</topic><topic>Epidermal cells</topic><topic>EPIDERME</topic><topic>EPIDERMIS</topic><topic>ESPORAS FUNGICAS</topic><topic>FUNGAL SPORES</topic><topic>Fungi</topic><topic>HYPHAE</topic><topic>INFECCION</topic><topic>INFECTION</topic><topic>KINETIN</topic><topic>KINETINE</topic><topic>LANTHANUM</topic><topic>LANTHANUM CHLORIDE</topic><topic>MECANISME DE DEFENSE</topic><topic>MECANISMOS DE DEFENSA</topic><topic>MEDICAMENTOS CARDIOVASCULARES</topic><topic>METAL DES TERRES RARES</topic><topic>MICELIO</topic><topic>MODIFICATEUR CARDIOVASCULAIRE</topic><topic>MYCELIUM</topic><topic>PARED CELULAR</topic><topic>PAROI CELLULAIRE</topic><topic>Plant cells</topic><topic>Plants</topic><topic>QUINETINA</topic><topic>RARE EARTH ELEMENTS</topic><topic>Ratio analysis</topic><topic>RESISTANCE AUX MALADIES</topic><topic>RESISTENCIA A LA ENFERMEDAD</topic><topic>ROUILLE</topic><topic>ROYA</topic><topic>RUSTS</topic><topic>SPORE FONGIQUE</topic><topic>TMB-8</topic><topic>UROMYCES APPENDICULATUS</topic><topic>VERAPAMIL</topic><topic>VIGNA UNGUICULATA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, H. (University of Toronto, Ontario, Canada.)</creatorcontrib><creatorcontrib>Heath, M.C</creatorcontrib><collection>AGRIS</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Plant cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, H. (University of Toronto, Ontario, Canada.)</au><au>Heath, M.C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus</atitle><jtitle>The Plant cell</jtitle><addtitle>Plant Cell</addtitle><date>1998-04-01</date><risdate>1998</risdate><volume>10</volume><issue>4</issue><spage>585</spage><epage>597</epage><pages>585-597</pages><issn>1040-4651</issn><eissn>1532-298X</eissn><abstract>The hypersensitive response (HR) of disease-resistant plant cells to fungal invasion is a rapid cell death that has some features in common with programmed cell death (apoptosis) in animals. We investigated the role of cytosolic free calcium ([Ca2+]i) in the HR of cowpea to the cowpea rust fungus. By using confocal laser scanning microscopy in conjunction with a calcium reporter dye, we found a slow, prolonged elevation of [Ca2+]i in epidermal cells of resistant but not susceptible plants as the fungus grew through the cell wall. [Ca2+]i levels declined to normal levels as the fungus entered and grew within the cell lumen. This elevation was related to the stage of fungal growth and not to the speed of initiation of subsequent cell death. Elevated [Ca2+]i levels also represent the first sign of the HR detectable in this cowpea-cowpea rust fungus system. The increase in [Ca2+]i was prevented by calcium channel inhibitors. This effect was consistent with pharmacological tests in which these inhibitors delayed the HR. The data suggest that elevation of [Ca2+]i is involved in signal transduction leading to the HR during rust fungal infection</abstract><cop>United States</cop><pub>American Society of Plant Physiologists</pub><pmid>9548984</pmid><doi>10.1105/tpc.10.4.585</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1040-4651 |
ispartof | The Plant cell, 1998-04, Vol.10 (4), p.585-597 |
issn | 1040-4651 1532-298X |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_144015 |
source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; JSTOR Archive Collection A-Z Listing; Oxford University Press Journals All Titles (1996-Current) |
subjects | ANTIMETABOLITE ANTIMETABOLITES ANTIMETABOLITOS BIOCHEMISTRY BIOCHIMIE BIOQUIMICA CALCIO CALCIUM CALCIUM CHANNEL INHIBITORS CARDIOVASCULAR AGENTS CATION CATIONES CATIONS Cell death Cell nucleus CELL WALLS CYTOCHEMISTRY DEFENCE MECHANISMS DISEASE RESISTANCE Dyes EGTA ELEMENTOS DE TIERRAS RARAS Epidermal cells EPIDERME EPIDERMIS ESPORAS FUNGICAS FUNGAL SPORES Fungi HYPHAE INFECCION INFECTION KINETIN KINETINE LANTHANUM LANTHANUM CHLORIDE MECANISME DE DEFENSE MECANISMOS DE DEFENSA MEDICAMENTOS CARDIOVASCULARES METAL DES TERRES RARES MICELIO MODIFICATEUR CARDIOVASCULAIRE MYCELIUM PARED CELULAR PAROI CELLULAIRE Plant cells Plants QUINETINA RARE EARTH ELEMENTS Ratio analysis RESISTANCE AUX MALADIES RESISTENCIA A LA ENFERMEDAD ROUILLE ROYA RUSTS SPORE FONGIQUE TMB-8 UROMYCES APPENDICULATUS VERAPAMIL VIGNA UNGUICULATA |
title | Role of calcium in signal transduction during the hypersensitive response caused by basidiospore-derived infection of the cowpea rust fungus |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-14T22%3A56%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-jstor_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Role%20of%20calcium%20in%20signal%20transduction%20during%20the%20hypersensitive%20response%20caused%20by%20basidiospore-derived%20infection%20of%20the%20cowpea%20rust%20fungus&rft.jtitle=The%20Plant%20cell&rft.au=Xu,%20H.%20(University%20of%20Toronto,%20Ontario,%20Canada.)&rft.date=1998-04-01&rft.volume=10&rft.issue=4&rft.spage=585&rft.epage=597&rft.pages=585-597&rft.issn=1040-4651&rft.eissn=1532-298X&rft_id=info:doi/10.1105/tpc.10.4.585&rft_dat=%3Cjstor_pubme%3E3870734%3C/jstor_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17572598&rft_id=info:pmid/9548984&rft_jstor_id=3870734&rfr_iscdi=true |