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Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation
Ustilago maydis is a biotrophic pathogen and well-established genetic model to understand the molecular basis of biotrophic interactions. U. maydis suppresses plant defense and induces tumors on all aerial parts of its host plant maize. In a previous study we found that U. maydis induced leaf tumor...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629649/ https://www.ncbi.nlm.nih.gov/pubmed/31308451 http://dx.doi.org/10.1038/s41598-019-46734-3 |
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author | Villajuana-Bonequi, Mitzi Matei, Alexandra Ernst, Corinna Hallab, Asis Usadel, Björn Doehlemann, Gunther |
author_facet | Villajuana-Bonequi, Mitzi Matei, Alexandra Ernst, Corinna Hallab, Asis Usadel, Björn Doehlemann, Gunther |
author_sort | Villajuana-Bonequi, Mitzi |
collection | PubMed |
description | Ustilago maydis is a biotrophic pathogen and well-established genetic model to understand the molecular basis of biotrophic interactions. U. maydis suppresses plant defense and induces tumors on all aerial parts of its host plant maize. In a previous study we found that U. maydis induced leaf tumor formation builds on two major processes: the induction of hypertrophy in the mesophyll and the induction of cell division (hyperplasia) in the bundle sheath. In this study we analyzed the cell-type specific transcriptome of maize leaves 4 days post infection. This analysis allowed identification of key features underlying the hypertrophic and hyperplasic cell identities derived from mesophyll and bundle sheath cells, respectively. We examined the differentially expressed (DE) genes with particular focus on maize cell cycle genes and found that three A-type cyclins, one B-, D- and T-type are upregulated in the hyperplasic tumorous cells, in which the U. maydis effector protein See1 promotes cell division. Additionally, most of the proteins involved in the formation of the pre-replication complex (pre-RC, that assure that each daughter cell receives identic DNA copies), the transcription factors E2F and DPa as well as several D-type cyclins are deregulated in the hypertrophic cells. |
format | Online Article Text |
id | pubmed-6629649 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-66296492019-07-23 Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation Villajuana-Bonequi, Mitzi Matei, Alexandra Ernst, Corinna Hallab, Asis Usadel, Björn Doehlemann, Gunther Sci Rep Article Ustilago maydis is a biotrophic pathogen and well-established genetic model to understand the molecular basis of biotrophic interactions. U. maydis suppresses plant defense and induces tumors on all aerial parts of its host plant maize. In a previous study we found that U. maydis induced leaf tumor formation builds on two major processes: the induction of hypertrophy in the mesophyll and the induction of cell division (hyperplasia) in the bundle sheath. In this study we analyzed the cell-type specific transcriptome of maize leaves 4 days post infection. This analysis allowed identification of key features underlying the hypertrophic and hyperplasic cell identities derived from mesophyll and bundle sheath cells, respectively. We examined the differentially expressed (DE) genes with particular focus on maize cell cycle genes and found that three A-type cyclins, one B-, D- and T-type are upregulated in the hyperplasic tumorous cells, in which the U. maydis effector protein See1 promotes cell division. Additionally, most of the proteins involved in the formation of the pre-replication complex (pre-RC, that assure that each daughter cell receives identic DNA copies), the transcription factors E2F and DPa as well as several D-type cyclins are deregulated in the hypertrophic cells. Nature Publishing Group UK 2019-07-15 /pmc/articles/PMC6629649/ /pubmed/31308451 http://dx.doi.org/10.1038/s41598-019-46734-3 Text en © The Author(s) 2019 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/. |
spellingShingle | Article Villajuana-Bonequi, Mitzi Matei, Alexandra Ernst, Corinna Hallab, Asis Usadel, Björn Doehlemann, Gunther Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title | Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title_full | Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title_fullStr | Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title_full_unstemmed | Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title_short | Cell type specific transcriptional reprogramming of maize leaves during Ustilago maydis induced tumor formation |
title_sort | cell type specific transcriptional reprogramming of maize leaves during ustilago maydis induced tumor formation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6629649/ https://www.ncbi.nlm.nih.gov/pubmed/31308451 http://dx.doi.org/10.1038/s41598-019-46734-3 |
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