Loading…

Bax-induced cell death in tobacco is similar to the hypersensitive response

Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-ter...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1999-07, Vol.96 (14), p.7956-7961
Main Authors: Lacomme, C, Santa Cruz, S
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563
cites cdi_FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563
container_end_page 7961
container_issue 14
container_start_page 7956
container_title Proceedings of the National Academy of Sciences - PNAS
container_volume 96
creator Lacomme, C
Santa Cruz, S
description Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.
doi_str_mv 10.1073/pnas.96.14.7956
format article
fullrecord <record><control><sourceid>jstor_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_22169</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><jstor_id>48408</jstor_id><sourcerecordid>48408</sourcerecordid><originalsourceid>FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563</originalsourceid><addsrcrecordid>eNp9kc1v1DAUxC0EokvhjMQBLA5wyvY9fySxxAWq8iEqcYCeLa_jdL3KxsF2qva_b0JKteXAyZLnN08zGkJeIqwRKn4y9CatVblGsa6ULB-RFYLCohQKHpMVAKuKWjBxRJ6ltAMAJWt4So4QuOKKqRX5_slcF75vRusaal3X0caZvKW-pzlsjLWB-kST3_vOxOmL5q2j25vBxeT65LO_cjS6NIQ-uefkSWu65F7cvcfk4vPZr9OvxfmPL99OP54XtgSVi1ZWxoqqNso4pqpKAm6QCcklM4jSWm6lbJoNq1GCEK20DsFBaxmIlsuSH5MPy91h3OxdY12fo-n0EP3exBsdjNcPld5v9WW40oxhqSb7uzt7DL9Hl7Le-zRXN70LY9JYsRJRzODbf8BdGGM_VdMMkAvO_kAnC2RjSCm69j4Hgp430vNGWpUahZ43mhyvD-Mf8MsoB8Ds_Cs_uPD-v4Bux67L7jpP5KuF3KUc4j0qagH1JL5ZxNYEbS6jT_ri59wMphCsrhS_BfaNt8Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>201343249</pqid></control><display><type>article</type><title>Bax-induced cell death in tobacco is similar to the hypersensitive response</title><source>PubMed Central (Open access)</source><source>JSTOR Archival Journals and Primary Sources Collection【Remote access available】</source><creator>Lacomme, C ; Santa Cruz, S</creator><creatorcontrib>Lacomme, C ; Santa Cruz, S</creatorcontrib><description>Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.96.14.7956</identifier><identifier>PMID: 10393929</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>Animals ; Apoptosis ; bcl-2-Associated X Protein ; Biological Sciences ; carboxylic acids ; Cell death ; Cellular biology ; comparisons ; Complementary DNA ; defense mechanisms ; deletions ; disease resistance ; experimental infections ; Flowers &amp; plants ; Genes ; Green Fluorescent Proteins ; Infections ; Leaves ; Lesions ; Luminescent Proteins - genetics ; Mice ; Microscopy, Confocal ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - physiology ; Mitochondria - ultrastructure ; mutants ; n gene ; Nicotiana ; Nicotiana - cytology ; Nicotiana - physiology ; Nicotiana benthamiana ; nicotiana edwardsonii ; Nicotiana tabacum ; Nucleocapsid Proteins - genetics ; Nucleocapsid Proteins - physiology ; okadaic acid ; Okadaic Acid - pharmacology ; pathogenesis-related proteins ; Phenotype ; Plant cells ; plant proteins ; Plants ; Plants, Toxic ; protein synthesis ; Proteins ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-bcl-2 ; Tobacco ; Tobacco mosaic virus ; Tobacco Mosaic Virus - genetics ; Tobacco Mosaic Virus - physiology ; Transcription, Genetic ; transgenic plants ; Viruses ; Yeasts</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1999-07, Vol.96 (14), p.7956-7961</ispartof><rights>Copyright 1993-1999 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jul 6, 1999</rights><rights>Copyright © 1999, The National Academy of Sciences 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563</citedby><cites>FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/96/14.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/48408$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/48408$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793,58238,58471</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10393929$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lacomme, C</creatorcontrib><creatorcontrib>Santa Cruz, S</creatorcontrib><title>Bax-induced cell death in tobacco is similar to the hypersensitive response</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological Sciences</subject><subject>carboxylic acids</subject><subject>Cell death</subject><subject>Cellular biology</subject><subject>comparisons</subject><subject>Complementary DNA</subject><subject>defense mechanisms</subject><subject>deletions</subject><subject>disease resistance</subject><subject>experimental infections</subject><subject>Flowers &amp; plants</subject><subject>Genes</subject><subject>Green Fluorescent Proteins</subject><subject>Infections</subject><subject>Leaves</subject><subject>Lesions</subject><subject>Luminescent Proteins - genetics</subject><subject>Mice</subject><subject>Microscopy, Confocal</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - physiology</subject><subject>Mitochondria - ultrastructure</subject><subject>mutants</subject><subject>n gene</subject><subject>Nicotiana</subject><subject>Nicotiana - cytology</subject><subject>Nicotiana - physiology</subject><subject>Nicotiana benthamiana</subject><subject>nicotiana edwardsonii</subject><subject>Nicotiana tabacum</subject><subject>Nucleocapsid Proteins - genetics</subject><subject>Nucleocapsid Proteins - physiology</subject><subject>okadaic acid</subject><subject>Okadaic Acid - pharmacology</subject><subject>pathogenesis-related proteins</subject><subject>Phenotype</subject><subject>Plant cells</subject><subject>plant proteins</subject><subject>Plants</subject><subject>Plants, Toxic</subject><subject>protein synthesis</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Tobacco</subject><subject>Tobacco mosaic virus</subject><subject>Tobacco Mosaic Virus - genetics</subject><subject>Tobacco Mosaic Virus - physiology</subject><subject>Transcription, Genetic</subject><subject>transgenic plants</subject><subject>Viruses</subject><subject>Yeasts</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNp9kc1v1DAUxC0EokvhjMQBLA5wyvY9fySxxAWq8iEqcYCeLa_jdL3KxsF2qva_b0JKteXAyZLnN08zGkJeIqwRKn4y9CatVblGsa6ULB-RFYLCohQKHpMVAKuKWjBxRJ6ltAMAJWt4So4QuOKKqRX5_slcF75vRusaal3X0caZvKW-pzlsjLWB-kST3_vOxOmL5q2j25vBxeT65LO_cjS6NIQ-uefkSWu65F7cvcfk4vPZr9OvxfmPL99OP54XtgSVi1ZWxoqqNso4pqpKAm6QCcklM4jSWm6lbJoNq1GCEK20DsFBaxmIlsuSH5MPy91h3OxdY12fo-n0EP3exBsdjNcPld5v9WW40oxhqSb7uzt7DL9Hl7Le-zRXN70LY9JYsRJRzODbf8BdGGM_VdMMkAvO_kAnC2RjSCm69j4Hgp430vNGWpUahZ43mhyvD-Mf8MsoB8Ds_Cs_uPD-v4Bux67L7jpP5KuF3KUc4j0qagH1JL5ZxNYEbS6jT_ri59wMphCsrhS_BfaNt8Q</recordid><startdate>19990706</startdate><enddate>19990706</enddate><creator>Lacomme, C</creator><creator>Santa Cruz, S</creator><general>National Academy of Sciences of the United States of America</general><general>National Acad Sciences</general><general>National Academy of Sciences</general><general>The National Academy of Sciences</general><scope>FBQ</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>19990706</creationdate><title>Bax-induced cell death in tobacco is similar to the hypersensitive response</title><author>Lacomme, C ; Santa Cruz, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological Sciences</topic><topic>carboxylic acids</topic><topic>Cell death</topic><topic>Cellular biology</topic><topic>comparisons</topic><topic>Complementary DNA</topic><topic>defense mechanisms</topic><topic>deletions</topic><topic>disease resistance</topic><topic>experimental infections</topic><topic>Flowers &amp; plants</topic><topic>Genes</topic><topic>Green Fluorescent Proteins</topic><topic>Infections</topic><topic>Leaves</topic><topic>Lesions</topic><topic>Luminescent Proteins - genetics</topic><topic>Mice</topic><topic>Microscopy, Confocal</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - physiology</topic><topic>Mitochondria - ultrastructure</topic><topic>mutants</topic><topic>n gene</topic><topic>Nicotiana</topic><topic>Nicotiana - cytology</topic><topic>Nicotiana - physiology</topic><topic>Nicotiana benthamiana</topic><topic>nicotiana edwardsonii</topic><topic>Nicotiana tabacum</topic><topic>Nucleocapsid Proteins - genetics</topic><topic>Nucleocapsid Proteins - physiology</topic><topic>okadaic acid</topic><topic>Okadaic Acid - pharmacology</topic><topic>pathogenesis-related proteins</topic><topic>Phenotype</topic><topic>Plant cells</topic><topic>plant proteins</topic><topic>Plants</topic><topic>Plants, Toxic</topic><topic>protein synthesis</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Tobacco</topic><topic>Tobacco mosaic virus</topic><topic>Tobacco Mosaic Virus - genetics</topic><topic>Tobacco Mosaic Virus - physiology</topic><topic>Transcription, Genetic</topic><topic>transgenic plants</topic><topic>Viruses</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lacomme, C</creatorcontrib><creatorcontrib>Santa Cruz, S</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lacomme, C</au><au>Santa Cruz, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bax-induced cell death in tobacco is similar to the hypersensitive response</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1999-07-06</date><risdate>1999</risdate><volume>96</volume><issue>14</issue><spage>7956</spage><epage>7961</epage><pages>7956-7961</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Bax, a death-promoting member of the Bcl-2 family of proteins, triggered cell death when expressed in plants from a tobacco mosaic virus vector. Analysis of Bax deletion mutants demonstrated a requirement for the BH1 and BH3 domains in promoting rapid cell death, whereas deletion of the carboxyl-terminal transmembrane domain completely abolished the lethality of Bax in plants. The phenotype of cell death induced by Bax closely resembled the hypersensitive response induced by wild-type tobacco mosaic virus in tobacco plants carrying the N gene. The cell death-promoting function of Bax in plants correlated with accumulation of the defense-related protein PR1, suggesting Bax activated an endogenous cell-death program in plants. In support of this view, both N gene- and Bax-mediated cell death was blocked by okadaic acid, an inhibitor of protein phosphatase activity. The ability of Bax to induce cell death and a defense reaction in plants suggests that some features of animal and plant cell death processes may be shared.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>10393929</pmid><doi>10.1073/pnas.96.14.7956</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0027-8424
ispartof Proceedings of the National Academy of Sciences - PNAS, 1999-07, Vol.96 (14), p.7956-7961
issn 0027-8424
1091-6490
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_22169
source PubMed Central (Open access); JSTOR Archival Journals and Primary Sources Collection【Remote access available】
subjects Animals
Apoptosis
bcl-2-Associated X Protein
Biological Sciences
carboxylic acids
Cell death
Cellular biology
comparisons
Complementary DNA
defense mechanisms
deletions
disease resistance
experimental infections
Flowers & plants
Genes
Green Fluorescent Proteins
Infections
Leaves
Lesions
Luminescent Proteins - genetics
Mice
Microscopy, Confocal
Mitochondria
Mitochondria - drug effects
Mitochondria - physiology
Mitochondria - ultrastructure
mutants
n gene
Nicotiana
Nicotiana - cytology
Nicotiana - physiology
Nicotiana benthamiana
nicotiana edwardsonii
Nicotiana tabacum
Nucleocapsid Proteins - genetics
Nucleocapsid Proteins - physiology
okadaic acid
Okadaic Acid - pharmacology
pathogenesis-related proteins
Phenotype
Plant cells
plant proteins
Plants
Plants, Toxic
protein synthesis
Proteins
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins - physiology
Proto-Oncogene Proteins c-bcl-2
Tobacco
Tobacco mosaic virus
Tobacco Mosaic Virus - genetics
Tobacco Mosaic Virus - physiology
Transcription, Genetic
transgenic plants
Viruses
Yeasts
title Bax-induced cell death in tobacco is similar to the hypersensitive response
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T08%3A23%3A18IST&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=Bax-induced%20cell%20death%20in%20tobacco%20is%20similar%20to%20the%20hypersensitive%20response&rft.jtitle=Proceedings%20of%20the%20National%20Academy%20of%20Sciences%20-%20PNAS&rft.au=Lacomme,%20C&rft.date=1999-07-06&rft.volume=96&rft.issue=14&rft.spage=7956&rft.epage=7961&rft.pages=7956-7961&rft.issn=0027-8424&rft.eissn=1091-6490&rft_id=info:doi/10.1073/pnas.96.14.7956&rft_dat=%3Cjstor_pubme%3E48408%3C/jstor_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c609t-f57ac478a9ae2977501b1245352a115cc3c55ddb2815044f5ce10e0fc204f3563%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=201343249&rft_id=info:pmid/10393929&rft_jstor_id=48408&rfr_iscdi=true