CbCTB2, an O-methyltransferase is essential for biosynthesis of the phytotoxin cercosporin and infection of sugar beet by Cercospora beticola
Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beets (Beta vulgaris) worldwide. Cercosporin, a light-inducible toxin, is essential for necrosis of the leaf tissue and development of the typical leaf spots on sugar beet leaves....
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description | Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beets (Beta vulgaris) worldwide. Cercosporin, a light-inducible toxin, is essential for necrosis of the leaf tissue and development of the typical leaf spots on sugar beet leaves.
In this study we show that the O-methyltransferase gene CTB2 is essential for cercosporin production and pathogenicity in two C. beticola isolates. We established a transformation system for C. beticola protoplasts, disrupted CTB2, and transformed the Δctb2 strains as well as a wild type strain with the DsRed reporter gene. The Δctb2 strains had lost their pigmentation and toxin measurements demonstrated that the Δctb2 strains were defective in cercosporin production. Infection of sugar beets with the wild type and Δctb2 DsRed strains showed that the deletion strain was severely impaired in plant infection. Histological analysis revealed that the CTB2-deficient isolate cannot enter the leaf tissue through stomata like the wild type.
Taken together, these observations indicate that cercosporin has a dual function in sugar beet infection: in addition to the well-known role in tissue necrosis, the toxin is required for the early phase of sugar beet infection. |
doi_str_mv | 10.1186/1471-2229-13-50 |
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In this study we show that the O-methyltransferase gene CTB2 is essential for cercosporin production and pathogenicity in two C. beticola isolates. We established a transformation system for C. beticola protoplasts, disrupted CTB2, and transformed the Δctb2 strains as well as a wild type strain with the DsRed reporter gene. The Δctb2 strains had lost their pigmentation and toxin measurements demonstrated that the Δctb2 strains were defective in cercosporin production. Infection of sugar beets with the wild type and Δctb2 DsRed strains showed that the deletion strain was severely impaired in plant infection. Histological analysis revealed that the CTB2-deficient isolate cannot enter the leaf tissue through stomata like the wild type.
Taken together, these observations indicate that cercosporin has a dual function in sugar beet infection: in addition to the well-known role in tissue necrosis, the toxin is required for the early phase of sugar beet infection.</description><identifier>ISSN: 1471-2229</identifier><identifier>EISSN: 1471-2229</identifier><identifier>DOI: 10.1186/1471-2229-13-50</identifier><identifier>PMID: 23517289</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Ascomycota ; Ascomycota - enzymology ; Ascomycota - genetics ; Ascomycota - pathogenicity ; Beta vulgaris ; Beta vulgaris - microbiology ; Biosynthesis ; Cercospora beticola ; Foliar diseases ; fungal diseases of plants ; Fungi ; Genes ; Genetic aspects ; Health aspects ; infection ; Infections ; leaf spot ; Leaves ; Light ; Methyltransferases ; Microscopy ; necrosis ; pathogenicity ; Perylene - analogs & derivatives ; Perylene - metabolism ; Physiological aspects ; pigmentation ; Plant Diseases - microbiology ; plant pathogenic fungi ; protoplasts ; reporter genes ; stomata ; Sugar beet ; Toxins ; Transferases</subject><ispartof>BMC plant biology, 2013-03, Vol.13 (1), p.50-50, Article 50</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Staerkel et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Staerkel et al.; licensee BioMed Central Ltd. 2013 Staerkel et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b647t-cd189c10611b7394170d48fa51c39d56d05cfeb7adde023aad83d7bf207b93c3</citedby><cites>FETCH-LOGICAL-b647t-cd189c10611b7394170d48fa51c39d56d05cfeb7adde023aad83d7bf207b93c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616835/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3616835/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23517289$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Staerkel, Cornelia</creatorcontrib><creatorcontrib>Boenisch, Marike J</creatorcontrib><creatorcontrib>Kröger, Cathrin</creatorcontrib><creatorcontrib>Bormann, Jörg</creatorcontrib><creatorcontrib>Schäfer, Wilhelm</creatorcontrib><creatorcontrib>Stahl, Dietmar</creatorcontrib><title>CbCTB2, an O-methyltransferase is essential for biosynthesis of the phytotoxin cercosporin and infection of sugar beet by Cercospora beticola</title><title>BMC plant biology</title><addtitle>BMC Plant Biol</addtitle><description>Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beets (Beta vulgaris) worldwide. Cercosporin, a light-inducible toxin, is essential for necrosis of the leaf tissue and development of the typical leaf spots on sugar beet leaves.
In this study we show that the O-methyltransferase gene CTB2 is essential for cercosporin production and pathogenicity in two C. beticola isolates. We established a transformation system for C. beticola protoplasts, disrupted CTB2, and transformed the Δctb2 strains as well as a wild type strain with the DsRed reporter gene. The Δctb2 strains had lost their pigmentation and toxin measurements demonstrated that the Δctb2 strains were defective in cercosporin production. Infection of sugar beets with the wild type and Δctb2 DsRed strains showed that the deletion strain was severely impaired in plant infection. Histological analysis revealed that the CTB2-deficient isolate cannot enter the leaf tissue through stomata like the wild type.
Taken together, these observations indicate that cercosporin has a dual function in sugar beet infection: in addition to the well-known role in tissue necrosis, the toxin is required for the early phase of sugar beet infection.</description><subject>Analysis</subject><subject>Ascomycota</subject><subject>Ascomycota - enzymology</subject><subject>Ascomycota - genetics</subject><subject>Ascomycota - pathogenicity</subject><subject>Beta vulgaris</subject><subject>Beta vulgaris - microbiology</subject><subject>Biosynthesis</subject><subject>Cercospora beticola</subject><subject>Foliar diseases</subject><subject>fungal diseases of plants</subject><subject>Fungi</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>infection</subject><subject>Infections</subject><subject>leaf spot</subject><subject>Leaves</subject><subject>Light</subject><subject>Methyltransferases</subject><subject>Microscopy</subject><subject>necrosis</subject><subject>pathogenicity</subject><subject>Perylene - analogs & derivatives</subject><subject>Perylene - metabolism</subject><subject>Physiological aspects</subject><subject>pigmentation</subject><subject>Plant Diseases - microbiology</subject><subject>plant pathogenic fungi</subject><subject>protoplasts</subject><subject>reporter genes</subject><subject>stomata</subject><subject>Sugar beet</subject><subject>Toxins</subject><subject>Transferases</subject><issn>1471-2229</issn><issn>1471-2229</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFk11rHCEUhofS0qRpr3tXhN600En8HJ2bQLL0IxAItLkXR51dw4xu1SnZH9H_XIdNttmSEgQ9nPP4oufVqnqL4DFCojlBlKMaY9zWiNQMPqsOd5nnD-KD6lVKNxAiLmj7sjrAhCGORXtY_V50i-tz_AkoD67q0ebVZshR-dTbqJIFLgGbkvXZqQH0IYLOhbTxeWVTKYUelAisV5sccrh1HmgbdUjrEEusvAHO91ZnF_zMpmmpioK1GXQbsLhHVUllp8OgXlcvejUk--ZuPaquv3y-XnyrL6--XizOLuuuoTzX2iDRagQbhDpOWoo4NFT0iiFNWsMaA5nubceVMRZiopQRxPCux5B3LdHkqDrdyq6nbrRGl-tFNch1dKOKGxmUk_sV71ZyGX5J0qBGEFYEzrcCpRv_Ediv6DDK2Q05uyERkQwWkQ93p4jh52RTlqNL2g6D8jZMSWJYDKOi2PQkimhDGWKck6dRgikRbYNEQd__g96EKfrS-JkiFLIy_6WWarCy-BnKjfQsKs8YoYwLzGmhjh-hyjB2LNZ627uS39vwcW9DYbK9zUs1pSQvfnzfZ0-2rI4hpWj7XacRlPM_eKS37x46vOPvHz75Aw-0AvQ</recordid><startdate>20130322</startdate><enddate>20130322</enddate><creator>Staerkel, Cornelia</creator><creator>Boenisch, Marike J</creator><creator>Kröger, Cathrin</creator><creator>Bormann, Jörg</creator><creator>Schäfer, Wilhelm</creator><creator>Stahl, Dietmar</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ISR</scope><scope>3V.</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20130322</creationdate><title>CbCTB2, an O-methyltransferase is essential for biosynthesis of the phytotoxin cercosporin and infection of sugar beet by Cercospora beticola</title><author>Staerkel, Cornelia ; Boenisch, Marike J ; Kröger, Cathrin ; Bormann, Jörg ; Schäfer, Wilhelm ; Stahl, Dietmar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b647t-cd189c10611b7394170d48fa51c39d56d05cfeb7adde023aad83d7bf207b93c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Analysis</topic><topic>Ascomycota</topic><topic>Ascomycota - enzymology</topic><topic>Ascomycota - genetics</topic><topic>Ascomycota - pathogenicity</topic><topic>Beta vulgaris</topic><topic>Beta vulgaris - microbiology</topic><topic>Biosynthesis</topic><topic>Cercospora beticola</topic><topic>Foliar diseases</topic><topic>fungal diseases of plants</topic><topic>Fungi</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>infection</topic><topic>Infections</topic><topic>leaf spot</topic><topic>Leaves</topic><topic>Light</topic><topic>Methyltransferases</topic><topic>Microscopy</topic><topic>necrosis</topic><topic>pathogenicity</topic><topic>Perylene - analogs & derivatives</topic><topic>Perylene - metabolism</topic><topic>Physiological aspects</topic><topic>pigmentation</topic><topic>Plant Diseases - microbiology</topic><topic>plant pathogenic fungi</topic><topic>protoplasts</topic><topic>reporter genes</topic><topic>stomata</topic><topic>Sugar beet</topic><topic>Toxins</topic><topic>Transferases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Staerkel, Cornelia</creatorcontrib><creatorcontrib>Boenisch, Marike J</creatorcontrib><creatorcontrib>Kröger, Cathrin</creatorcontrib><creatorcontrib>Bormann, Jörg</creatorcontrib><creatorcontrib>Schäfer, Wilhelm</creatorcontrib><creatorcontrib>Stahl, Dietmar</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC plant biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Staerkel, Cornelia</au><au>Boenisch, Marike J</au><au>Kröger, Cathrin</au><au>Bormann, Jörg</au><au>Schäfer, Wilhelm</au><au>Stahl, Dietmar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CbCTB2, an O-methyltransferase is essential for biosynthesis of the phytotoxin cercosporin and infection of sugar beet by Cercospora beticola</atitle><jtitle>BMC plant biology</jtitle><addtitle>BMC Plant Biol</addtitle><date>2013-03-22</date><risdate>2013</risdate><volume>13</volume><issue>1</issue><spage>50</spage><epage>50</epage><pages>50-50</pages><artnum>50</artnum><issn>1471-2229</issn><eissn>1471-2229</eissn><abstract>Cercospora leaf spot disease, caused by the fungus Cercospora beticola, is the most destructive foliar disease of sugar beets (Beta vulgaris) worldwide. Cercosporin, a light-inducible toxin, is essential for necrosis of the leaf tissue and development of the typical leaf spots on sugar beet leaves.
In this study we show that the O-methyltransferase gene CTB2 is essential for cercosporin production and pathogenicity in two C. beticola isolates. We established a transformation system for C. beticola protoplasts, disrupted CTB2, and transformed the Δctb2 strains as well as a wild type strain with the DsRed reporter gene. The Δctb2 strains had lost their pigmentation and toxin measurements demonstrated that the Δctb2 strains were defective in cercosporin production. Infection of sugar beets with the wild type and Δctb2 DsRed strains showed that the deletion strain was severely impaired in plant infection. Histological analysis revealed that the CTB2-deficient isolate cannot enter the leaf tissue through stomata like the wild type.
Taken together, these observations indicate that cercosporin has a dual function in sugar beet infection: in addition to the well-known role in tissue necrosis, the toxin is required for the early phase of sugar beet infection.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23517289</pmid><doi>10.1186/1471-2229-13-50</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Ascomycota Ascomycota - enzymology Ascomycota - genetics Ascomycota - pathogenicity Beta vulgaris Beta vulgaris - microbiology Biosynthesis Cercospora beticola Foliar diseases fungal diseases of plants Fungi Genes Genetic aspects Health aspects infection Infections leaf spot Leaves Light Methyltransferases Microscopy necrosis pathogenicity Perylene - analogs & derivatives Perylene - metabolism Physiological aspects pigmentation Plant Diseases - microbiology plant pathogenic fungi protoplasts reporter genes stomata Sugar beet Toxins Transferases |
title | CbCTB2, an O-methyltransferase is essential for biosynthesis of the phytotoxin cercosporin and infection of sugar beet by Cercospora beticola |
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