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Investigation of the effects of P1 on HC-pro-mediated gene silencing suppression through genetics and omics approaches
Background Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The...
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Published in: | Botanical studies 2020-08, Vol.61 (1), p.22-22, Article 22 |
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creator | Hu, Sin-Fen Wei, Wei-Lun Hong, Syuan-Fei Fang, Ru-Ying Wu, Hsin-Yi Lin, Pin-Chun Sanobar, Neda Wang, Hsin-Ping Sulistio, Margo Wu, Chun-Ta Lo, Hsiao-Feng Lin, Shih-Shun |
description | Background
Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The first identified viral suppressor, P1/HC-Pro, is a fusion protein that was translated from potyviral RNA. Upon infecting plants, the P1 protein itself is released from HC-Pro by the self-cleaving activity of P1. P1 has an unknown function in enhancing HC-Pro-mediated PTGS suppression. We performed proteomics to identify P1-interacting proteins. We also performed transcriptomics that were generated from Col-0 and various P1/HC-Pro-related transgenic plants to identify novel genes. The results showed several novel genes were identified through the comparative network analysis that might be involved in P1/HC-Pro-mediated PTGS suppression.
Results
First, we demonstrated that P1 enhances HC-Pro function and that the mechanism might work through P1 binding to VERNALIZATION INDEPENDENCE 3/SUPERKILLER 8 (VIP3/SKI8), a subunit of the exosome, to interfere with the 5
′
-fragment of the PTGS-cleaved RNA degradation product. Second, the AGO1 was specifically posttranslationally degraded in transgenic Arabidopsis expressing
P1/HC
-
Pro
of turnip mosaic virus (TuMV) (
P1/HC
Tu
plant). Third, the comparative network highlighted potentially critical genes in PTGS, including miRNA targets, calcium signaling, hormone (JA, ET, and ABA) signaling, and defense response.
Conclusion
Through these genetic and omics approaches, we revealed an overall perspective to identify many critical genes involved in PTGS. These new findings significantly impact in our understanding of P1/HC-Pro-mediated PTGS suppression. |
doi_str_mv | 10.1186/s40529-020-00299-x |
format | article |
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Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The first identified viral suppressor, P1/HC-Pro, is a fusion protein that was translated from potyviral RNA. Upon infecting plants, the P1 protein itself is released from HC-Pro by the self-cleaving activity of P1. P1 has an unknown function in enhancing HC-Pro-mediated PTGS suppression. We performed proteomics to identify P1-interacting proteins. We also performed transcriptomics that were generated from Col-0 and various P1/HC-Pro-related transgenic plants to identify novel genes. The results showed several novel genes were identified through the comparative network analysis that might be involved in P1/HC-Pro-mediated PTGS suppression.
Results
First, we demonstrated that P1 enhances HC-Pro function and that the mechanism might work through P1 binding to VERNALIZATION INDEPENDENCE 3/SUPERKILLER 8 (VIP3/SKI8), a subunit of the exosome, to interfere with the 5
′
-fragment of the PTGS-cleaved RNA degradation product. Second, the AGO1 was specifically posttranslationally degraded in transgenic Arabidopsis expressing
P1/HC
-
Pro
of turnip mosaic virus (TuMV) (
P1/HC
Tu
plant). Third, the comparative network highlighted potentially critical genes in PTGS, including miRNA targets, calcium signaling, hormone (JA, ET, and ABA) signaling, and defense response.
Conclusion
Through these genetic and omics approaches, we revealed an overall perspective to identify many critical genes involved in PTGS. These new findings significantly impact in our understanding of P1/HC-Pro-mediated PTGS suppression.</description><identifier>ISSN: 1999-3110</identifier><identifier>ISSN: 1817-406X</identifier><identifier>EISSN: 1999-3110</identifier><identifier>DOI: 10.1186/s40529-020-00299-x</identifier><identifier>PMID: 32748085</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Abscisic acid ; Biomedical and Life Sciences ; Calcium ; Calcium signalling ; Comparative network ; Ecology ; Fusion protein ; Gene silencing ; Genes ; Genetics ; Life Sciences ; MicroRNA ; MicroRNAs ; miRNA ; Molecular Biology ; Network analysis ; Omics ; Original ; Original Article ; p1 Protein ; P1/HC-Pro ; Plant Genetics and Genomics ; Plant Sciences ; Post-transcription ; Posttranscriptional gene silencing ; Proteins ; Proteomics ; Ribonucleic acid ; RNA ; Signaling ; siRNA ; Suppressors ; Transcriptomics ; Transgenic plants ; Vernalization ; Viral suppressor ; Viruses</subject><ispartof>Botanical studies, 2020-08, Vol.61 (1), p.22-22, Article 22</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c684t-6ccf25ae7671edf12949b28dcc952aa28d36b37ef46e0bf9ec032f1110d360dd3</citedby><cites>FETCH-LOGICAL-c684t-6ccf25ae7671edf12949b28dcc952aa28d36b37ef46e0bf9ec032f1110d360dd3</cites><orcidid>0000-0002-7295-5004</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2429921975/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2429921975?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,25734,27905,27906,36993,36994,44571,53772,53774,74875</link.rule.ids></links><search><creatorcontrib>Hu, Sin-Fen</creatorcontrib><creatorcontrib>Wei, Wei-Lun</creatorcontrib><creatorcontrib>Hong, Syuan-Fei</creatorcontrib><creatorcontrib>Fang, Ru-Ying</creatorcontrib><creatorcontrib>Wu, Hsin-Yi</creatorcontrib><creatorcontrib>Lin, Pin-Chun</creatorcontrib><creatorcontrib>Sanobar, Neda</creatorcontrib><creatorcontrib>Wang, Hsin-Ping</creatorcontrib><creatorcontrib>Sulistio, Margo</creatorcontrib><creatorcontrib>Wu, Chun-Ta</creatorcontrib><creatorcontrib>Lo, Hsiao-Feng</creatorcontrib><creatorcontrib>Lin, Shih-Shun</creatorcontrib><title>Investigation of the effects of P1 on HC-pro-mediated gene silencing suppression through genetics and omics approaches</title><title>Botanical studies</title><addtitle>Bot Stud</addtitle><description>Background
Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The first identified viral suppressor, P1/HC-Pro, is a fusion protein that was translated from potyviral RNA. Upon infecting plants, the P1 protein itself is released from HC-Pro by the self-cleaving activity of P1. P1 has an unknown function in enhancing HC-Pro-mediated PTGS suppression. We performed proteomics to identify P1-interacting proteins. We also performed transcriptomics that were generated from Col-0 and various P1/HC-Pro-related transgenic plants to identify novel genes. The results showed several novel genes were identified through the comparative network analysis that might be involved in P1/HC-Pro-mediated PTGS suppression.
Results
First, we demonstrated that P1 enhances HC-Pro function and that the mechanism might work through P1 binding to VERNALIZATION INDEPENDENCE 3/SUPERKILLER 8 (VIP3/SKI8), a subunit of the exosome, to interfere with the 5
′
-fragment of the PTGS-cleaved RNA degradation product. Second, the AGO1 was specifically posttranslationally degraded in transgenic Arabidopsis expressing
P1/HC
-
Pro
of turnip mosaic virus (TuMV) (
P1/HC
Tu
plant). Third, the comparative network highlighted potentially critical genes in PTGS, including miRNA targets, calcium signaling, hormone (JA, ET, and ABA) signaling, and defense response.
Conclusion
Through these genetic and omics approaches, we revealed an overall perspective to identify many critical genes involved in PTGS. These new findings significantly impact in our understanding of P1/HC-Pro-mediated PTGS suppression.</description><subject>Abscisic acid</subject><subject>Biomedical and Life Sciences</subject><subject>Calcium</subject><subject>Calcium signalling</subject><subject>Comparative network</subject><subject>Ecology</subject><subject>Fusion protein</subject><subject>Gene silencing</subject><subject>Genes</subject><subject>Genetics</subject><subject>Life Sciences</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Molecular Biology</subject><subject>Network analysis</subject><subject>Omics</subject><subject>Original</subject><subject>Original Article</subject><subject>p1 Protein</subject><subject>P1/HC-Pro</subject><subject>Plant Genetics and Genomics</subject><subject>Plant Sciences</subject><subject>Post-transcription</subject><subject>Posttranscriptional gene silencing</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signaling</subject><subject>siRNA</subject><subject>Suppressors</subject><subject>Transcriptomics</subject><subject>Transgenic plants</subject><subject>Vernalization</subject><subject>Viral suppressor</subject><subject>Viruses</subject><issn>1999-3110</issn><issn>1817-406X</issn><issn>1999-3110</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9ks-P1SAQxxujcX_oP-CpiRcvXWFoabmYmBd1X7KJHvRMKAxtX_qgQvuy-99LXzfqevDEMHznwzB8s-wNJTeUNvx9LEkFoiBACkJAiOL-WXZJRQoYpeT5X_FFdhXjgRBOgcHL7IJBXTakqS6z096dMM5Dp-bBu9zbfO4xR2tRz3HdfqN5yt_uiin44ohmUDOavEOHeRxGdHpwXR6XaQoY44qY--CXrj9L5kHHXDmT--M5SiqvdI_xVfbCqjHi68f1Ovvx-dP33W1x9_XLfvfxrtC8KeeCa22hUljzmqKxFEQpWmiM1qICpVLEeMtqtCVH0lqBmjCwNL04HRBj2HW237jGq4OcwnBU4UF6NchzwodOqpC6HFEaqoCUFIyxOt1SNWBbXQOA4qThmibWh401LW0ahEY3BzU-gT49cUMvO3-SNROiZlUCvHsEBP9zSVOXxyFqHEfl0C9RQskI4w0Xq_TtP9KDX4JLo0qq9NVARb2qYFPp4GMMaH83Q4lcLSI3i8hkEXm2iLxPRWwriknsOgx_0P-p-gVTNL_Y</recordid><startdate>20200803</startdate><enddate>20200803</enddate><creator>Hu, Sin-Fen</creator><creator>Wei, Wei-Lun</creator><creator>Hong, Syuan-Fei</creator><creator>Fang, Ru-Ying</creator><creator>Wu, Hsin-Yi</creator><creator>Lin, Pin-Chun</creator><creator>Sanobar, Neda</creator><creator>Wang, Hsin-Ping</creator><creator>Sulistio, Margo</creator><creator>Wu, Chun-Ta</creator><creator>Lo, Hsiao-Feng</creator><creator>Lin, Shih-Shun</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><general>SpringerOpen</general><scope>C6C</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X2</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M0K</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-7295-5004</orcidid></search><sort><creationdate>20200803</creationdate><title>Investigation of the effects of P1 on HC-pro-mediated gene silencing suppression through genetics and omics approaches</title><author>Hu, Sin-Fen ; Wei, Wei-Lun ; Hong, Syuan-Fei ; Fang, Ru-Ying ; Wu, Hsin-Yi ; Lin, Pin-Chun ; Sanobar, Neda ; Wang, Hsin-Ping ; Sulistio, Margo ; Wu, Chun-Ta ; Lo, Hsiao-Feng ; Lin, Shih-Shun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c684t-6ccf25ae7671edf12949b28dcc952aa28d36b37ef46e0bf9ec032f1110d360dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Abscisic acid</topic><topic>Biomedical and Life Sciences</topic><topic>Calcium</topic><topic>Calcium signalling</topic><topic>Comparative network</topic><topic>Ecology</topic><topic>Fusion protein</topic><topic>Gene silencing</topic><topic>Genes</topic><topic>Genetics</topic><topic>Life Sciences</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Molecular Biology</topic><topic>Network analysis</topic><topic>Omics</topic><topic>Original</topic><topic>Original Article</topic><topic>p1 Protein</topic><topic>P1/HC-Pro</topic><topic>Plant Genetics and Genomics</topic><topic>Plant Sciences</topic><topic>Post-transcription</topic><topic>Posttranscriptional gene silencing</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signaling</topic><topic>siRNA</topic><topic>Suppressors</topic><topic>Transcriptomics</topic><topic>Transgenic plants</topic><topic>Vernalization</topic><topic>Viral suppressor</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hu, Sin-Fen</creatorcontrib><creatorcontrib>Wei, Wei-Lun</creatorcontrib><creatorcontrib>Hong, Syuan-Fei</creatorcontrib><creatorcontrib>Fang, Ru-Ying</creatorcontrib><creatorcontrib>Wu, Hsin-Yi</creatorcontrib><creatorcontrib>Lin, Pin-Chun</creatorcontrib><creatorcontrib>Sanobar, Neda</creatorcontrib><creatorcontrib>Wang, Hsin-Ping</creatorcontrib><creatorcontrib>Sulistio, Margo</creatorcontrib><creatorcontrib>Wu, Chun-Ta</creatorcontrib><creatorcontrib>Lo, Hsiao-Feng</creatorcontrib><creatorcontrib>Lin, Shih-Shun</creatorcontrib><collection>SpringerOpen</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Agricultural Science Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</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>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agriculture Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Botanical studies</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hu, Sin-Fen</au><au>Wei, Wei-Lun</au><au>Hong, Syuan-Fei</au><au>Fang, Ru-Ying</au><au>Wu, Hsin-Yi</au><au>Lin, Pin-Chun</au><au>Sanobar, Neda</au><au>Wang, Hsin-Ping</au><au>Sulistio, Margo</au><au>Wu, Chun-Ta</au><au>Lo, Hsiao-Feng</au><au>Lin, Shih-Shun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Investigation of the effects of P1 on HC-pro-mediated gene silencing suppression through genetics and omics approaches</atitle><jtitle>Botanical studies</jtitle><stitle>Bot Stud</stitle><date>2020-08-03</date><risdate>2020</risdate><volume>61</volume><issue>1</issue><spage>22</spage><epage>22</epage><pages>22-22</pages><artnum>22</artnum><issn>1999-3110</issn><issn>1817-406X</issn><eissn>1999-3110</eissn><abstract>Background
Posttranscriptional gene silencing (PTGS) is one of the most important mechanisms for plants during viral infection. However, viruses have also developed viral suppressors to negatively control PTGS by inhibiting microRNA (miRNA) and short-interfering RNA (siRNA) regulation in plants. The first identified viral suppressor, P1/HC-Pro, is a fusion protein that was translated from potyviral RNA. Upon infecting plants, the P1 protein itself is released from HC-Pro by the self-cleaving activity of P1. P1 has an unknown function in enhancing HC-Pro-mediated PTGS suppression. We performed proteomics to identify P1-interacting proteins. We also performed transcriptomics that were generated from Col-0 and various P1/HC-Pro-related transgenic plants to identify novel genes. The results showed several novel genes were identified through the comparative network analysis that might be involved in P1/HC-Pro-mediated PTGS suppression.
Results
First, we demonstrated that P1 enhances HC-Pro function and that the mechanism might work through P1 binding to VERNALIZATION INDEPENDENCE 3/SUPERKILLER 8 (VIP3/SKI8), a subunit of the exosome, to interfere with the 5
′
-fragment of the PTGS-cleaved RNA degradation product. Second, the AGO1 was specifically posttranslationally degraded in transgenic Arabidopsis expressing
P1/HC
-
Pro
of turnip mosaic virus (TuMV) (
P1/HC
Tu
plant). Third, the comparative network highlighted potentially critical genes in PTGS, including miRNA targets, calcium signaling, hormone (JA, ET, and ABA) signaling, and defense response.
Conclusion
Through these genetic and omics approaches, we revealed an overall perspective to identify many critical genes involved in PTGS. These new findings significantly impact in our understanding of P1/HC-Pro-mediated PTGS suppression.</abstract><cop>Singapore</cop><pub>Springer Singapore</pub><pmid>32748085</pmid><doi>10.1186/s40529-020-00299-x</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-7295-5004</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Abscisic acid Biomedical and Life Sciences Calcium Calcium signalling Comparative network Ecology Fusion protein Gene silencing Genes Genetics Life Sciences MicroRNA MicroRNAs miRNA Molecular Biology Network analysis Omics Original Original Article p1 Protein P1/HC-Pro Plant Genetics and Genomics Plant Sciences Post-transcription Posttranscriptional gene silencing Proteins Proteomics Ribonucleic acid RNA Signaling siRNA Suppressors Transcriptomics Transgenic plants Vernalization Viral suppressor Viruses |
title | Investigation of the effects of P1 on HC-pro-mediated gene silencing suppression through genetics and omics approaches |
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