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WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis
Wounding triggers de novo organogenesis, vascular reconnection and defense response but how wound stress evoke such a diverse array of physiological responses remains unknown. We previously identified AP2/ERF transcription factors, WOUND INDUCED DEDIFFERENTIATION1 (WIND1) and its homologs, WIND2, WI...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9291923/ https://www.ncbi.nlm.nih.gov/pubmed/34375004 http://dx.doi.org/10.1111/nph.17594 |
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author | Iwase, Akira Kondo, Yuki Laohavisit, Anuphon Takebayashi, Arika Ikeuchi, Momoko Matsuoka, Keita Asahina, Masashi Mitsuda, Nobutaka Shirasu, Ken Fukuda, Hiroo Sugimoto, Keiko |
author_facet | Iwase, Akira Kondo, Yuki Laohavisit, Anuphon Takebayashi, Arika Ikeuchi, Momoko Matsuoka, Keita Asahina, Masashi Mitsuda, Nobutaka Shirasu, Ken Fukuda, Hiroo Sugimoto, Keiko |
author_sort | Iwase, Akira |
collection | PubMed |
description | Wounding triggers de novo organogenesis, vascular reconnection and defense response but how wound stress evoke such a diverse array of physiological responses remains unknown. We previously identified AP2/ERF transcription factors, WOUND INDUCED DEDIFFERENTIATION1 (WIND1) and its homologs, WIND2, WIND3 and WIND4, as key regulators of wound‐induced cellular reprogramming in Arabidopsis. To understand how WIND transcription factors promote downstream events, we performed time‐course transcriptome analyses after WIND1 induction. We observed a significant overlap between WIND1‐induced genes and genes implicated in cellular reprogramming, vascular formation and pathogen response. We demonstrated that WIND transcription factors induce several reprogramming genes to promote callus formation at wound sites. We, in addition, showed that WIND transcription factors promote tracheary element formation, vascular reconnection and resistance to Pseudomonas syringae pv. tomato DC3000. These results indicate that WIND transcription factors function as key regulators of wound‐induced responses by promoting dynamic transcriptional alterations. This study provides deeper mechanistic insights into how plants control multiple physiological responses after wounding. |
format | Online Article Text |
id | pubmed-9291923 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-92919232022-07-20 WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis Iwase, Akira Kondo, Yuki Laohavisit, Anuphon Takebayashi, Arika Ikeuchi, Momoko Matsuoka, Keita Asahina, Masashi Mitsuda, Nobutaka Shirasu, Ken Fukuda, Hiroo Sugimoto, Keiko New Phytol Research Wounding triggers de novo organogenesis, vascular reconnection and defense response but how wound stress evoke such a diverse array of physiological responses remains unknown. We previously identified AP2/ERF transcription factors, WOUND INDUCED DEDIFFERENTIATION1 (WIND1) and its homologs, WIND2, WIND3 and WIND4, as key regulators of wound‐induced cellular reprogramming in Arabidopsis. To understand how WIND transcription factors promote downstream events, we performed time‐course transcriptome analyses after WIND1 induction. We observed a significant overlap between WIND1‐induced genes and genes implicated in cellular reprogramming, vascular formation and pathogen response. We demonstrated that WIND transcription factors induce several reprogramming genes to promote callus formation at wound sites. We, in addition, showed that WIND transcription factors promote tracheary element formation, vascular reconnection and resistance to Pseudomonas syringae pv. tomato DC3000. These results indicate that WIND transcription factors function as key regulators of wound‐induced responses by promoting dynamic transcriptional alterations. This study provides deeper mechanistic insights into how plants control multiple physiological responses after wounding. John Wiley and Sons Inc. 2021-08-10 2021-10 /pmc/articles/PMC9291923/ /pubmed/34375004 http://dx.doi.org/10.1111/nph.17594 Text en © 2021 The Authors. New Phytologist © 2021 New Phytologist Foundation https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Research Iwase, Akira Kondo, Yuki Laohavisit, Anuphon Takebayashi, Arika Ikeuchi, Momoko Matsuoka, Keita Asahina, Masashi Mitsuda, Nobutaka Shirasu, Ken Fukuda, Hiroo Sugimoto, Keiko WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title | WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title_full | WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title_fullStr | WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title_full_unstemmed | WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title_short | WIND transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in Arabidopsis |
title_sort | wind transcription factors orchestrate wound‐induced callus formation, vascular reconnection and defense response in arabidopsis |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9291923/ https://www.ncbi.nlm.nih.gov/pubmed/34375004 http://dx.doi.org/10.1111/nph.17594 |
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