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Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis
Plasmodiophora brassicae is a soil‐borne biotroph whose life cycle involves reprogramming host developmental processes leading to the formation of galls on its underground parts. Formation of such structures involves modification of the host cell cycle leading initially to hyperplasia, increasing th...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850046/ https://www.ncbi.nlm.nih.gov/pubmed/30431210 http://dx.doi.org/10.1111/tpj.14156 |
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author | Olszak, Marcin Truman, William Stefanowicz, Karolina Sliwinska, Elwira Ito, Masaki Walerowski, Piotr Rolfe, Stephen Malinowski, Robert |
author_facet | Olszak, Marcin Truman, William Stefanowicz, Karolina Sliwinska, Elwira Ito, Masaki Walerowski, Piotr Rolfe, Stephen Malinowski, Robert |
author_sort | Olszak, Marcin |
collection | PubMed |
description | Plasmodiophora brassicae is a soil‐borne biotroph whose life cycle involves reprogramming host developmental processes leading to the formation of galls on its underground parts. Formation of such structures involves modification of the host cell cycle leading initially to hyperplasia, increasing the number of cells to be invaded, followed by overgrowth of cells colonised by the pathogen. Here we show that P. brassicae infection stimulates formation of the E2Fa/RBR1 complex and upregulation of MYB3R1,MYB3R4 and A‐ and B‐type cyclin expression. These factors were previously described as important regulators of the G2−M cell cycle checkpoint. As a consequence of this manipulation, a large population of host hypocotyl cells are delayed in cell cycle exit and maintained in the proliferative state. We also report that, during further maturation of galls, enlargement of host cells invaded by the pathogen involves endoreduplication leading to increased ploidy levels. This study characterises two aspects of the cell cycle reprogramming efforts of P. brassicae: systemic, related to the disturbance of host hypocotyl developmental programs by preventing cell cycle exit; and local, related to the stimulation of cell enlargement via increased endocycle activity. |
format | Online Article Text |
id | pubmed-6850046 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68500462019-11-15 Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis Olszak, Marcin Truman, William Stefanowicz, Karolina Sliwinska, Elwira Ito, Masaki Walerowski, Piotr Rolfe, Stephen Malinowski, Robert Plant J Original Articles Plasmodiophora brassicae is a soil‐borne biotroph whose life cycle involves reprogramming host developmental processes leading to the formation of galls on its underground parts. Formation of such structures involves modification of the host cell cycle leading initially to hyperplasia, increasing the number of cells to be invaded, followed by overgrowth of cells colonised by the pathogen. Here we show that P. brassicae infection stimulates formation of the E2Fa/RBR1 complex and upregulation of MYB3R1,MYB3R4 and A‐ and B‐type cyclin expression. These factors were previously described as important regulators of the G2−M cell cycle checkpoint. As a consequence of this manipulation, a large population of host hypocotyl cells are delayed in cell cycle exit and maintained in the proliferative state. We also report that, during further maturation of galls, enlargement of host cells invaded by the pathogen involves endoreduplication leading to increased ploidy levels. This study characterises two aspects of the cell cycle reprogramming efforts of P. brassicae: systemic, related to the disturbance of host hypocotyl developmental programs by preventing cell cycle exit; and local, related to the stimulation of cell enlargement via increased endocycle activity. John Wiley and Sons Inc. 2019-01-05 2019-02 /pmc/articles/PMC6850046/ /pubmed/30431210 http://dx.doi.org/10.1111/tpj.14156 Text en © 2018 The Authors The Plant Journal published by John Wiley & Sons Ltd and Society for Experimental Biology. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Olszak, Marcin Truman, William Stefanowicz, Karolina Sliwinska, Elwira Ito, Masaki Walerowski, Piotr Rolfe, Stephen Malinowski, Robert Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title | Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title_full | Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title_fullStr | Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title_full_unstemmed | Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title_short | Transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for Plasmodiophora brassicae‐driven gall formation in Arabidopsis |
title_sort | transcriptional profiling identifies critical steps of cell cycle reprogramming necessary for plasmodiophora brassicae‐driven gall formation in arabidopsis |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6850046/ https://www.ncbi.nlm.nih.gov/pubmed/30431210 http://dx.doi.org/10.1111/tpj.14156 |
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