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Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules

Azorhizobium caulinodans ORS571 is a diazotroph that forms N(2)-fixing nodules on the roots and stems of the tropical legume Sesbania rostrata. Deletion of the parA gene of this bacterium results in cell cycle defects, pleiomorphic cell shape, and formation of immature stem nodules on its host plant...

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Autores principales: Chien, Hsiao-Lin, Huang, Wan-Zhen, Tsai, Ming-Yen, Cheng, Chiung-Hsiang, Liu, Chi-Te
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842974/
https://www.ncbi.nlm.nih.gov/pubmed/31749773
http://dx.doi.org/10.3389/fmicb.2019.02422
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author Chien, Hsiao-Lin
Huang, Wan-Zhen
Tsai, Ming-Yen
Cheng, Chiung-Hsiang
Liu, Chi-Te
author_facet Chien, Hsiao-Lin
Huang, Wan-Zhen
Tsai, Ming-Yen
Cheng, Chiung-Hsiang
Liu, Chi-Te
author_sort Chien, Hsiao-Lin
collection PubMed
description Azorhizobium caulinodans ORS571 is a diazotroph that forms N(2)-fixing nodules on the roots and stems of the tropical legume Sesbania rostrata. Deletion of the parA gene of this bacterium results in cell cycle defects, pleiomorphic cell shape, and formation of immature stem nodules on its host plant. In this study, we constructed a parA overexpression mutant (PnptII-parA) to complement a previous study and provide new insights into bacteroid formation. We found that overproduction of ParA did not affect growth, cell morphology, chromosome partitioning, or vegetative nitrogen fixation in the free-living state. Under symbiosis, however, distinctive features, such as a single swollen bacteroid in one symbiosome, relatively narrow symbiosome space, and polyploid cells were observed. The morphotype of the PnptII-parA bacteroid is reminiscent of terminal differentiation in some IRLC indeterminate nodules, but S. rostrata is not thought to produce the NCR peptides that induce terminal differentiation in rhizobia. In addition, the transcript patterns of many symbiosis-related genes elicited by PnptII-parA were different from those elicited by the wild type. Accordingly, we propose that the particular symbiosome formation in PnptII-parA stem-nodules is due to cell cycle disruption caused by excess ParA protein in the symbiotic cells during nodulation.
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spelling pubmed-68429742019-11-20 Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules Chien, Hsiao-Lin Huang, Wan-Zhen Tsai, Ming-Yen Cheng, Chiung-Hsiang Liu, Chi-Te Front Microbiol Microbiology Azorhizobium caulinodans ORS571 is a diazotroph that forms N(2)-fixing nodules on the roots and stems of the tropical legume Sesbania rostrata. Deletion of the parA gene of this bacterium results in cell cycle defects, pleiomorphic cell shape, and formation of immature stem nodules on its host plant. In this study, we constructed a parA overexpression mutant (PnptII-parA) to complement a previous study and provide new insights into bacteroid formation. We found that overproduction of ParA did not affect growth, cell morphology, chromosome partitioning, or vegetative nitrogen fixation in the free-living state. Under symbiosis, however, distinctive features, such as a single swollen bacteroid in one symbiosome, relatively narrow symbiosome space, and polyploid cells were observed. The morphotype of the PnptII-parA bacteroid is reminiscent of terminal differentiation in some IRLC indeterminate nodules, but S. rostrata is not thought to produce the NCR peptides that induce terminal differentiation in rhizobia. In addition, the transcript patterns of many symbiosis-related genes elicited by PnptII-parA were different from those elicited by the wild type. Accordingly, we propose that the particular symbiosome formation in PnptII-parA stem-nodules is due to cell cycle disruption caused by excess ParA protein in the symbiotic cells during nodulation. Frontiers Media S.A. 2019-10-24 /pmc/articles/PMC6842974/ /pubmed/31749773 http://dx.doi.org/10.3389/fmicb.2019.02422 Text en Copyright © 2019 Chien, Huang, Tsai, Cheng and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Chien, Hsiao-Lin
Huang, Wan-Zhen
Tsai, Ming-Yen
Cheng, Chiung-Hsiang
Liu, Chi-Te
Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title_full Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title_fullStr Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title_full_unstemmed Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title_short Overexpression of the Chromosome Partitioning Gene parA in Azorhizobium caulinodans ORS571 Alters the Bacteroid Morphotype in Sesbania rostrata Stem Nodules
title_sort overexpression of the chromosome partitioning gene para in azorhizobium caulinodans ors571 alters the bacteroid morphotype in sesbania rostrata stem nodules
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6842974/
https://www.ncbi.nlm.nih.gov/pubmed/31749773
http://dx.doi.org/10.3389/fmicb.2019.02422
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