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A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation
Ustilago maydis causes common smut in maize, which is characterized by tumor formation in aerial parts of maize. Tumors result from the de novo cell division of highly developed bundle sheath and subsequent cell enlargement. However, the molecular mechanisms underlying tumorigenesis are still largel...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10593772/ https://www.ncbi.nlm.nih.gov/pubmed/37872143 http://dx.doi.org/10.1038/s41467-023-42522-w |
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author | Zuo, Weiliang Depotter, Jasper R. L. Stolze, Sara Christina Nakagami, Hirofumi Doehlemann, Gunther |
author_facet | Zuo, Weiliang Depotter, Jasper R. L. Stolze, Sara Christina Nakagami, Hirofumi Doehlemann, Gunther |
author_sort | Zuo, Weiliang |
collection | PubMed |
description | Ustilago maydis causes common smut in maize, which is characterized by tumor formation in aerial parts of maize. Tumors result from the de novo cell division of highly developed bundle sheath and subsequent cell enlargement. However, the molecular mechanisms underlying tumorigenesis are still largely unknown. Here, we characterize the U. maydis effector Sts2 (Small tumor on seedlings 2), which promotes the division of hyperplasia tumor cells. Upon infection, Sts2 is translocated into the maize cell nucleus, where it acts as a transcriptional activator, and the transactivation activity is crucial for its virulence function. Sts2 interacts with ZmNECAP1, a yet undescribed plant transcriptional activator, and it activates the expression of several leaf developmental regulators to potentiate tumor formation. On the contrary, fusion of a suppressive SRDX-motif to Sts2 causes dominant negative inhibition of tumor formation, underpinning the central role of Sts2 for tumorigenesis. Our results not only disclose the virulence mechanism of a tumorigenic effector, but also reveal the essential role of leaf developmental regulators in pathogen-induced tumor formation. |
format | Online Article Text |
id | pubmed-10593772 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-105937722023-10-25 A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation Zuo, Weiliang Depotter, Jasper R. L. Stolze, Sara Christina Nakagami, Hirofumi Doehlemann, Gunther Nat Commun Article Ustilago maydis causes common smut in maize, which is characterized by tumor formation in aerial parts of maize. Tumors result from the de novo cell division of highly developed bundle sheath and subsequent cell enlargement. However, the molecular mechanisms underlying tumorigenesis are still largely unknown. Here, we characterize the U. maydis effector Sts2 (Small tumor on seedlings 2), which promotes the division of hyperplasia tumor cells. Upon infection, Sts2 is translocated into the maize cell nucleus, where it acts as a transcriptional activator, and the transactivation activity is crucial for its virulence function. Sts2 interacts with ZmNECAP1, a yet undescribed plant transcriptional activator, and it activates the expression of several leaf developmental regulators to potentiate tumor formation. On the contrary, fusion of a suppressive SRDX-motif to Sts2 causes dominant negative inhibition of tumor formation, underpinning the central role of Sts2 for tumorigenesis. Our results not only disclose the virulence mechanism of a tumorigenic effector, but also reveal the essential role of leaf developmental regulators in pathogen-induced tumor formation. Nature Publishing Group UK 2023-10-23 /pmc/articles/PMC10593772/ /pubmed/37872143 http://dx.doi.org/10.1038/s41467-023-42522-w Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Zuo, Weiliang Depotter, Jasper R. L. Stolze, Sara Christina Nakagami, Hirofumi Doehlemann, Gunther A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title | A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title_full | A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title_fullStr | A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title_full_unstemmed | A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title_short | A transcriptional activator effector of Ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
title_sort | transcriptional activator effector of ustilago maydis regulates hyperplasia in maize during pathogen-induced tumor formation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10593772/ https://www.ncbi.nlm.nih.gov/pubmed/37872143 http://dx.doi.org/10.1038/s41467-023-42522-w |
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