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Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri

Citrus canker is an economically important disease that affects orange production in some of the most important producing areas around the world. It represents a great threat to the Brazilian and North American citriculture, particularly to the states of São Paulo and Florida, which together corresp...

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Autores principales: Sumares, Júlia A. P., Morão, Luana Galvão, Martins, Paula M. M., Martins, Daniela A. B., Gomes, Eleni, Belasque, José, Ferreira, Henrique
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831469/
https://www.ncbi.nlm.nih.gov/pubmed/26663580
http://dx.doi.org/10.1002/mbo3.323
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author Sumares, Júlia A. P.
Morão, Luana Galvão
Martins, Paula M. M.
Martins, Daniela A. B.
Gomes, Eleni
Belasque, José
Ferreira, Henrique
author_facet Sumares, Júlia A. P.
Morão, Luana Galvão
Martins, Paula M. M.
Martins, Daniela A. B.
Gomes, Eleni
Belasque, José
Ferreira, Henrique
author_sort Sumares, Júlia A. P.
collection PubMed
description Citrus canker is an economically important disease that affects orange production in some of the most important producing areas around the world. It represents a great threat to the Brazilian and North American citriculture, particularly to the states of São Paulo and Florida, which together correspond to the biggest orange juice producers in the world. The etiological agent of this disease is the Gram‐negative bacterium Xanthomonas citri subsp. citri (Xcc), which grows optimally in laboratory cultures at ~30°C. To investigate how temperatures differing from 30°C influence the development of Xcc, we subjected the bacterium to thermal stresses, and afterward scored its recovery capability. In addition, we analyzed cell morphology and some markers of essential cellular processes that could indicate the extent of the heat‐induced damage. We found that the exposure of Xcc to 37°C for a period of 6 h led to a cell cycle arrest at the division stage. Thermal stress might have also interfered with the DNA replication and/or the chromosome segregation apparatuses, since cells displayed an increased number of sister origins side‐by‐side within rods. Additionally, Xcc treated at 37°C was still able to induce citrus canker symptoms, showing that thermal stress did not affect the ability of Xcc to colonize the host citrus. At 40–42°C, Xcc lost viability and became unable to induce disease symptoms in citrus. Our results provide evidence about essential cellular mechanisms perturbed by temperature, and can be potentially explored as a new method for Xanthomonas citri synchronization in cell cycle studies, as well as for the sanitation of plant material.
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spelling pubmed-48314692016-04-20 Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri Sumares, Júlia A. P. Morão, Luana Galvão Martins, Paula M. M. Martins, Daniela A. B. Gomes, Eleni Belasque, José Ferreira, Henrique Microbiologyopen Original Research Citrus canker is an economically important disease that affects orange production in some of the most important producing areas around the world. It represents a great threat to the Brazilian and North American citriculture, particularly to the states of São Paulo and Florida, which together correspond to the biggest orange juice producers in the world. The etiological agent of this disease is the Gram‐negative bacterium Xanthomonas citri subsp. citri (Xcc), which grows optimally in laboratory cultures at ~30°C. To investigate how temperatures differing from 30°C influence the development of Xcc, we subjected the bacterium to thermal stresses, and afterward scored its recovery capability. In addition, we analyzed cell morphology and some markers of essential cellular processes that could indicate the extent of the heat‐induced damage. We found that the exposure of Xcc to 37°C for a period of 6 h led to a cell cycle arrest at the division stage. Thermal stress might have also interfered with the DNA replication and/or the chromosome segregation apparatuses, since cells displayed an increased number of sister origins side‐by‐side within rods. Additionally, Xcc treated at 37°C was still able to induce citrus canker symptoms, showing that thermal stress did not affect the ability of Xcc to colonize the host citrus. At 40–42°C, Xcc lost viability and became unable to induce disease symptoms in citrus. Our results provide evidence about essential cellular mechanisms perturbed by temperature, and can be potentially explored as a new method for Xanthomonas citri synchronization in cell cycle studies, as well as for the sanitation of plant material. John Wiley and Sons Inc. 2015-12-13 /pmc/articles/PMC4831469/ /pubmed/26663580 http://dx.doi.org/10.1002/mbo3.323 Text en © 2015 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (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 Research
Sumares, Júlia A. P.
Morão, Luana Galvão
Martins, Paula M. M.
Martins, Daniela A. B.
Gomes, Eleni
Belasque, José
Ferreira, Henrique
Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title_full Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title_fullStr Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title_full_unstemmed Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title_short Temperature stress promotes cell division arrest in Xanthomonas citri subsp. citri
title_sort temperature stress promotes cell division arrest in xanthomonas citri subsp. citri
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831469/
https://www.ncbi.nlm.nih.gov/pubmed/26663580
http://dx.doi.org/10.1002/mbo3.323
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