Endogenous salicylic acid suppresses de novo root regeneration from leaf explants
Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role o...
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creator | Tran, Sorrel Ison, Madalene Ferreira Dias, Nathália Cássia Ortega, Maria Andrea Chen, Yun-Fan Stephanie Peper, Alan Hu, Lanxi Xu, Dawei Mozaffari, Khadijeh Severns, Paul M Yao, Yao Tsai, Chung-Jui Teixeira, Paulo José Pereira Lima Yang, Li |
description | Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration. |
doi_str_mv | 10.1371/journal.pgen.1010636 |
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In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1010636</identifier><identifier>PMID: 36857386</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Arabidopsis - metabolism ; Arabidopsis Proteins - metabolism ; Auxin ; Biology and Life Sciences ; Biosynthesis ; Defense industry ; Dosage and administration ; Environmental aspects ; Experiments ; Explants ; Foliage plants ; Gene Expression Regulation, Plant ; Genes ; Genetic aspects ; Growth ; Instrument industry ; Leaves ; Organogenesis ; Pathogens ; Phenols ; Plant Growth Regulators - metabolism ; Plant Growth Regulators - pharmacology ; Plant hormones ; Plant Leaves - metabolism ; Plant Roots - genetics ; Plant Roots - metabolism ; Research and Analysis Methods ; Roots (Botany) ; Salicylic acid ; Salicylic Acid - metabolism ; Transcription factors ; Wounding</subject><ispartof>PLoS genetics, 2023-03, Vol.19 (3), p.e1010636-e1010636</ispartof><rights>Copyright: © 2023 Tran et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2023 Public Library of Science</rights><rights>2023 Tran et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 Tran et al 2023 Tran et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c727t-5a8f4beb7ed4b70e5a1a2e9de4eac828db147d6a6497e3d6fcc793316b9b6bb83</citedby><cites>FETCH-LOGICAL-c727t-5a8f4beb7ed4b70e5a1a2e9de4eac828db147d6a6497e3d6fcc793316b9b6bb83</cites><orcidid>0000-0002-2552-9635 ; 0000-0001-8434-6532 ; 0000-0002-8906-7070 ; 0000-0002-9282-7704 ; 0000-0002-1493-8871 ; 0000-0003-3665-544X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10010561/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10010561/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36857386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Köhler, Claudia</contributor><creatorcontrib>Tran, Sorrel</creatorcontrib><creatorcontrib>Ison, Madalene</creatorcontrib><creatorcontrib>Ferreira Dias, Nathália Cássia</creatorcontrib><creatorcontrib>Ortega, Maria Andrea</creatorcontrib><creatorcontrib>Chen, Yun-Fan Stephanie</creatorcontrib><creatorcontrib>Peper, Alan</creatorcontrib><creatorcontrib>Hu, Lanxi</creatorcontrib><creatorcontrib>Xu, Dawei</creatorcontrib><creatorcontrib>Mozaffari, Khadijeh</creatorcontrib><creatorcontrib>Severns, Paul M</creatorcontrib><creatorcontrib>Yao, Yao</creatorcontrib><creatorcontrib>Tsai, Chung-Jui</creatorcontrib><creatorcontrib>Teixeira, Paulo José Pereira Lima</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><title>Endogenous salicylic acid suppresses de novo root regeneration from leaf explants</title><title>PLoS genetics</title><addtitle>PLoS Genet</addtitle><description>Plants can regenerate new organs from damaged or detached tissues. In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. Our work elucidates a role of SA in regulating DNRR and suggests a potential link between biotic stress and tissue regeneration.</description><subject>Analysis</subject><subject>Arabidopsis - metabolism</subject><subject>Arabidopsis Proteins - metabolism</subject><subject>Auxin</subject><subject>Biology and Life Sciences</subject><subject>Biosynthesis</subject><subject>Defense industry</subject><subject>Dosage and administration</subject><subject>Environmental aspects</subject><subject>Experiments</subject><subject>Explants</subject><subject>Foliage plants</subject><subject>Gene Expression Regulation, Plant</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Growth</subject><subject>Instrument industry</subject><subject>Leaves</subject><subject>Organogenesis</subject><subject>Pathogens</subject><subject>Phenols</subject><subject>Plant Growth Regulators - metabolism</subject><subject>Plant Growth Regulators - pharmacology</subject><subject>Plant hormones</subject><subject>Plant Leaves - 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In the process of de novo root regeneration (DNRR), adventitious roots are frequently formed from the wound site on a detached leaf. Salicylic acid (SA) is a key phytohormone regulating plant defenses and stress responses. The role of SA and its acting mechanisms during de novo organogenesis is still unclear. Here, we found that endogenous SA inhibited the adventitious root formation after cutting. Free SA rapidly accumulated at the wound site, which was accompanied by an activation of SA response. SA receptors NPR3 and NPR4, but not NPR1, were required for DNRR. Wounding-elevated SA compromised the expression of AUX1, and subsequent transport of auxin to the wound site. A mutation in AUX1 abolished the enhanced DNRR in low SA mutants. 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subjects | Analysis Arabidopsis - metabolism Arabidopsis Proteins - metabolism Auxin Biology and Life Sciences Biosynthesis Defense industry Dosage and administration Environmental aspects Experiments Explants Foliage plants Gene Expression Regulation, Plant Genes Genetic aspects Growth Instrument industry Leaves Organogenesis Pathogens Phenols Plant Growth Regulators - metabolism Plant Growth Regulators - pharmacology Plant hormones Plant Leaves - metabolism Plant Roots - genetics Plant Roots - metabolism Research and Analysis Methods Roots (Botany) Salicylic acid Salicylic Acid - metabolism Transcription factors Wounding |
title | Endogenous salicylic acid suppresses de novo root regeneration from leaf explants |
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