Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells
Previously, effect of Al ions on calcium signaling was assessed in tobacco cells expressing a Ca 2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca 2+ channel protein from Arabidopsis thaliana, AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only chann...
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Veröffentlicht in: | Biochemical and biophysical research communications 2005-07, Vol.332 (3), p.823-830 |
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creator | Lin, Cun Yu, Yawei Kadono, Takashi Iwata, Michiaki Umemura, Kenji Furuichi, Takuya Kuse, Masaki Isobe, Minoru Yamamoto, Yoko Matsumoto, Hideaki Yoshizuka, Kazuharu Kawano, Tomonori |
description | Previously, effect of Al ions on calcium signaling was assessed in tobacco cells expressing a Ca
2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca
2+ channel protein from
Arabidopsis thaliana,
AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only channel known to be sensitive to Al and they are responsive to reactive oxygen species and cryptogein, a fungal elicitor protein. Thus, involvement of TPC1 channels in calcium signaling leading to development of plant defense mechanism has been suggested. Then, the use of Al as a specific inhibitor of TPC1-type plant calcium channels has been proposed. Here, using transgenic tobacco BY-2 cells expressing aequorin, we report on the evidence in support of the involvement of Al-sensitive signaling pathway requiring TPC1-type channel-dependent Ca
2+ influx in response to salicylic acid, a key plant defense-inducing agent, but not to an elicitor prepared from the cell wall of rice blast disease fungus
Magnaporthe grisea. In addition, involvement of Al-sensitive Ca
2+ channels in response to cold shock was also tested. The data suggested that the elicitor used here induces the Ca
2+ influx via Al-insensitive path, while salicylic acid and cold-shock-stimulate the influx of Ca
2+ via Al-sensitive mechanism. |
doi_str_mv | 10.1016/j.bbrc.2005.05.030 |
format | Article |
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2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca
2+ channel protein from
Arabidopsis thaliana,
AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only channel known to be sensitive to Al and they are responsive to reactive oxygen species and cryptogein, a fungal elicitor protein. Thus, involvement of TPC1 channels in calcium signaling leading to development of plant defense mechanism has been suggested. Then, the use of Al as a specific inhibitor of TPC1-type plant calcium channels has been proposed. Here, using transgenic tobacco BY-2 cells expressing aequorin, we report on the evidence in support of the involvement of Al-sensitive signaling pathway requiring TPC1-type channel-dependent Ca
2+ influx in response to salicylic acid, a key plant defense-inducing agent, but not to an elicitor prepared from the cell wall of rice blast disease fungus
Magnaporthe grisea. In addition, involvement of Al-sensitive Ca
2+ channels in response to cold shock was also tested. The data suggested that the elicitor used here induces the Ca
2+ influx via Al-insensitive path, while salicylic acid and cold-shock-stimulate the influx of Ca
2+ via Al-sensitive mechanism.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2005.05.030</identifier><identifier>PMID: 15913561</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Aequorin ; Aequorin - genetics ; Aequorin - metabolism ; Aluminum - pharmacology ; Arabidopsis thaliana ; Calcium Channels ; Calcium Signaling - drug effects ; Cation Transport Proteins - antagonists & inhibitors ; Cold shock ; Cold Temperature ; Ion Channels - antagonists & inhibitors ; Magnaporthe - chemistry ; Magnaporthe grisea ; Models, Biological ; Nicotiana - cytology ; Nicotiana - drug effects ; Nicotiana - metabolism ; Nicotiana tabacum ; Oryza sativa ; Plants, Genetically Modified ; Recombinant Proteins - genetics ; Recombinant Proteins - metabolism ; Salicylic acid ; Salicylic Acid - pharmacology</subject><ispartof>Biochemical and biophysical research communications, 2005-07, Vol.332 (3), p.823-830</ispartof><rights>2005 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-83fef35bdfce7431a4bc85e83c389e88cf353712e2f3295f66b73de8f7143353</citedby><cites>FETCH-LOGICAL-c416t-83fef35bdfce7431a4bc85e83c389e88cf353712e2f3295f66b73de8f7143353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbrc.2005.05.030$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15913561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Cun</creatorcontrib><creatorcontrib>Yu, Yawei</creatorcontrib><creatorcontrib>Kadono, Takashi</creatorcontrib><creatorcontrib>Iwata, Michiaki</creatorcontrib><creatorcontrib>Umemura, Kenji</creatorcontrib><creatorcontrib>Furuichi, Takuya</creatorcontrib><creatorcontrib>Kuse, Masaki</creatorcontrib><creatorcontrib>Isobe, Minoru</creatorcontrib><creatorcontrib>Yamamoto, Yoko</creatorcontrib><creatorcontrib>Matsumoto, Hideaki</creatorcontrib><creatorcontrib>Yoshizuka, Kazuharu</creatorcontrib><creatorcontrib>Kawano, Tomonori</creatorcontrib><title>Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Previously, effect of Al ions on calcium signaling was assessed in tobacco cells expressing a Ca
2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca
2+ channel protein from
Arabidopsis thaliana,
AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only channel known to be sensitive to Al and they are responsive to reactive oxygen species and cryptogein, a fungal elicitor protein. Thus, involvement of TPC1 channels in calcium signaling leading to development of plant defense mechanism has been suggested. Then, the use of Al as a specific inhibitor of TPC1-type plant calcium channels has been proposed. Here, using transgenic tobacco BY-2 cells expressing aequorin, we report on the evidence in support of the involvement of Al-sensitive signaling pathway requiring TPC1-type channel-dependent Ca
2+ influx in response to salicylic acid, a key plant defense-inducing agent, but not to an elicitor prepared from the cell wall of rice blast disease fungus
Magnaporthe grisea. In addition, involvement of Al-sensitive Ca
2+ channels in response to cold shock was also tested. The data suggested that the elicitor used here induces the Ca
2+ influx via Al-insensitive path, while salicylic acid and cold-shock-stimulate the influx of Ca
2+ via Al-sensitive mechanism.</description><subject>Aequorin</subject><subject>Aequorin - genetics</subject><subject>Aequorin - metabolism</subject><subject>Aluminum - pharmacology</subject><subject>Arabidopsis thaliana</subject><subject>Calcium Channels</subject><subject>Calcium Signaling - drug effects</subject><subject>Cation Transport Proteins - antagonists & inhibitors</subject><subject>Cold shock</subject><subject>Cold Temperature</subject><subject>Ion Channels - antagonists & inhibitors</subject><subject>Magnaporthe - chemistry</subject><subject>Magnaporthe grisea</subject><subject>Models, Biological</subject><subject>Nicotiana - cytology</subject><subject>Nicotiana - drug effects</subject><subject>Nicotiana - metabolism</subject><subject>Nicotiana tabacum</subject><subject>Oryza sativa</subject><subject>Plants, Genetically Modified</subject><subject>Recombinant Proteins - genetics</subject><subject>Recombinant Proteins - metabolism</subject><subject>Salicylic acid</subject><subject>Salicylic Acid - pharmacology</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2LFDEQhoO4uOPqH_AgOXnaHvPRn-BlHfyChd3DHPQU0tUVJ2M6GTvpxfkR-59NM4PeFAoK6n3qpaiXkFecrTnj9dv9uu8nWAvGqvVSkj0hK846VgjOyqdkxRirC9Hxr5fkeYx7xjgv6-4ZueRVx2VV8xV5vIFkg6fBUO3m0fp5vKY-PKCj2_sNL9LxgBR22vs8sX5ne5vCdE31d219TDRqZ-HodMLC-mEGHKj2A4XghiLuAvz4MwbtwM5jNjFu_pUbTaHXAIG-_1YICuhcfEEujHYRX577Fdl-_LDdfC5u7z592dzcFlDyOhWtNGhk1Q8GsCkl12UPbYWtBNl22LaQRdlwgcJI0VWmrvtGDtiahpcyS1fkzcn2MIWfM8akRhuXA7THMEclWCMaJsR_Qd7IsqtYm0FxAmEKMU5o1GGyo56OijO1hKX2aglLLWGppSTLS6_P7nM_4vB35ZxOBt6dAMy_eLA4qQgWff6mnRCSGoL9l_9vuMGmhA</recordid><startdate>20050708</startdate><enddate>20050708</enddate><creator>Lin, Cun</creator><creator>Yu, Yawei</creator><creator>Kadono, Takashi</creator><creator>Iwata, Michiaki</creator><creator>Umemura, Kenji</creator><creator>Furuichi, Takuya</creator><creator>Kuse, Masaki</creator><creator>Isobe, Minoru</creator><creator>Yamamoto, Yoko</creator><creator>Matsumoto, Hideaki</creator><creator>Yoshizuka, Kazuharu</creator><creator>Kawano, Tomonori</creator><general>Elsevier Inc</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>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20050708</creationdate><title>Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells</title><author>Lin, Cun ; Yu, Yawei ; Kadono, Takashi ; Iwata, Michiaki ; Umemura, Kenji ; Furuichi, Takuya ; Kuse, Masaki ; Isobe, Minoru ; Yamamoto, Yoko ; Matsumoto, Hideaki ; Yoshizuka, Kazuharu ; Kawano, Tomonori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-83fef35bdfce7431a4bc85e83c389e88cf353712e2f3295f66b73de8f7143353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aequorin</topic><topic>Aequorin - genetics</topic><topic>Aequorin - metabolism</topic><topic>Aluminum - pharmacology</topic><topic>Arabidopsis thaliana</topic><topic>Calcium Channels</topic><topic>Calcium Signaling - drug effects</topic><topic>Cation Transport Proteins - antagonists & inhibitors</topic><topic>Cold shock</topic><topic>Cold Temperature</topic><topic>Ion Channels - antagonists & inhibitors</topic><topic>Magnaporthe - chemistry</topic><topic>Magnaporthe grisea</topic><topic>Models, Biological</topic><topic>Nicotiana - cytology</topic><topic>Nicotiana - drug effects</topic><topic>Nicotiana - metabolism</topic><topic>Nicotiana tabacum</topic><topic>Oryza sativa</topic><topic>Plants, Genetically Modified</topic><topic>Recombinant Proteins - genetics</topic><topic>Recombinant Proteins - metabolism</topic><topic>Salicylic acid</topic><topic>Salicylic Acid - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Cun</creatorcontrib><creatorcontrib>Yu, Yawei</creatorcontrib><creatorcontrib>Kadono, Takashi</creatorcontrib><creatorcontrib>Iwata, Michiaki</creatorcontrib><creatorcontrib>Umemura, Kenji</creatorcontrib><creatorcontrib>Furuichi, Takuya</creatorcontrib><creatorcontrib>Kuse, Masaki</creatorcontrib><creatorcontrib>Isobe, Minoru</creatorcontrib><creatorcontrib>Yamamoto, Yoko</creatorcontrib><creatorcontrib>Matsumoto, Hideaki</creatorcontrib><creatorcontrib>Yoshizuka, Kazuharu</creatorcontrib><creatorcontrib>Kawano, Tomonori</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</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><collection>Genetics Abstracts</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Cun</au><au>Yu, Yawei</au><au>Kadono, Takashi</au><au>Iwata, Michiaki</au><au>Umemura, Kenji</au><au>Furuichi, Takuya</au><au>Kuse, Masaki</au><au>Isobe, Minoru</au><au>Yamamoto, Yoko</au><au>Matsumoto, Hideaki</au><au>Yoshizuka, Kazuharu</au><au>Kawano, Tomonori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2005-07-08</date><risdate>2005</risdate><volume>332</volume><issue>3</issue><spage>823</spage><epage>830</epage><pages>823-830</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Previously, effect of Al ions on calcium signaling was assessed in tobacco cells expressing a Ca
2+-monitoring luminescent protein, aequorin and a newly isolated putative plant Ca
2+ channel protein from
Arabidopsis thaliana,
AtTPC1 (two-pore channel 1). TPC1 channels were shown to be the only channel known to be sensitive to Al and they are responsive to reactive oxygen species and cryptogein, a fungal elicitor protein. Thus, involvement of TPC1 channels in calcium signaling leading to development of plant defense mechanism has been suggested. Then, the use of Al as a specific inhibitor of TPC1-type plant calcium channels has been proposed. Here, using transgenic tobacco BY-2 cells expressing aequorin, we report on the evidence in support of the involvement of Al-sensitive signaling pathway requiring TPC1-type channel-dependent Ca
2+ influx in response to salicylic acid, a key plant defense-inducing agent, but not to an elicitor prepared from the cell wall of rice blast disease fungus
Magnaporthe grisea. In addition, involvement of Al-sensitive Ca
2+ channels in response to cold shock was also tested. The data suggested that the elicitor used here induces the Ca
2+ influx via Al-insensitive path, while salicylic acid and cold-shock-stimulate the influx of Ca
2+ via Al-sensitive mechanism.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>15913561</pmid><doi>10.1016/j.bbrc.2005.05.030</doi><tpages>8</tpages></addata></record> |
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subjects | Aequorin Aequorin - genetics Aequorin - metabolism Aluminum - pharmacology Arabidopsis thaliana Calcium Channels Calcium Signaling - drug effects Cation Transport Proteins - antagonists & inhibitors Cold shock Cold Temperature Ion Channels - antagonists & inhibitors Magnaporthe - chemistry Magnaporthe grisea Models, Biological Nicotiana - cytology Nicotiana - drug effects Nicotiana - metabolism Nicotiana tabacum Oryza sativa Plants, Genetically Modified Recombinant Proteins - genetics Recombinant Proteins - metabolism Salicylic acid Salicylic Acid - pharmacology |
title | Action of aluminum, novel TPC1-type channel inhibitor, against salicylate-induced and cold-shock-induced calcium influx in tobacco BY-2 cells |
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