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Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function
The plant cell wall is a highly dynamic structure that changes in response to both environmental and developmental cues. It plays important roles throughout plant growth and development in determining the orientation and extent of cell expansion, providing structural support and acting as a barrier...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032291/ https://www.ncbi.nlm.nih.gov/pubmed/24859261 http://dx.doi.org/10.1371/journal.pone.0098193 |
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author | Steinwand, Blaire J. Xu, Shouling Polko, Joanna K. Doctor, Stephanie M. Westafer, Mike Kieber, Joseph J. |
author_facet | Steinwand, Blaire J. Xu, Shouling Polko, Joanna K. Doctor, Stephanie M. Westafer, Mike Kieber, Joseph J. |
author_sort | Steinwand, Blaire J. |
collection | PubMed |
description | The plant cell wall is a highly dynamic structure that changes in response to both environmental and developmental cues. It plays important roles throughout plant growth and development in determining the orientation and extent of cell expansion, providing structural support and acting as a barrier to pathogens. Despite the importance of the cell wall, the signaling pathways regulating its function are not well understood. Two partially redundant leucine-rich-repeat receptor-like kinases (LRR-RLKs), FEI1 and FEI2, regulate cell wall function in Arabidopsis thaliana roots; disruption of the FEIs results in short, swollen roots as a result of decreased cellulose synthesis. We screened for suppressors of this swollen root phenotype and identified two mutations in the putative mitochondrial pyruvate dehydrogenase E1α homolog, IAA-Alanine Resistant 4 (IAR4). Mutations in IAR4 were shown previously to disrupt auxin homeostasis and lead to reduced auxin function. We show that mutations in IAR4 suppress a subset of the fei1 fei2 phenotypes. Consistent with the hypothesis that the suppression of fei1 fei2 by iar4 is the result of reduced auxin function, disruption of the WEI8 and TAR2 genes, which decreases auxin biosynthesis, also suppresses fei1 fei2. In addition, iar4 suppresses the root swelling and accumulation of ectopic lignin phenotypes of other cell wall mutants, including procuste and cobra. Further, iar4 mutants display decreased sensitivity to the cellulose biosynthesis inhibitor isoxaben. These results establish a role for IAR4 in the regulation of cell wall function and provide evidence of crosstalk between the cell wall and auxin during cell expansion in the root. |
format | Online Article Text |
id | pubmed-4032291 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-40322912014-05-28 Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function Steinwand, Blaire J. Xu, Shouling Polko, Joanna K. Doctor, Stephanie M. Westafer, Mike Kieber, Joseph J. PLoS One Research Article The plant cell wall is a highly dynamic structure that changes in response to both environmental and developmental cues. It plays important roles throughout plant growth and development in determining the orientation and extent of cell expansion, providing structural support and acting as a barrier to pathogens. Despite the importance of the cell wall, the signaling pathways regulating its function are not well understood. Two partially redundant leucine-rich-repeat receptor-like kinases (LRR-RLKs), FEI1 and FEI2, regulate cell wall function in Arabidopsis thaliana roots; disruption of the FEIs results in short, swollen roots as a result of decreased cellulose synthesis. We screened for suppressors of this swollen root phenotype and identified two mutations in the putative mitochondrial pyruvate dehydrogenase E1α homolog, IAA-Alanine Resistant 4 (IAR4). Mutations in IAR4 were shown previously to disrupt auxin homeostasis and lead to reduced auxin function. We show that mutations in IAR4 suppress a subset of the fei1 fei2 phenotypes. Consistent with the hypothesis that the suppression of fei1 fei2 by iar4 is the result of reduced auxin function, disruption of the WEI8 and TAR2 genes, which decreases auxin biosynthesis, also suppresses fei1 fei2. In addition, iar4 suppresses the root swelling and accumulation of ectopic lignin phenotypes of other cell wall mutants, including procuste and cobra. Further, iar4 mutants display decreased sensitivity to the cellulose biosynthesis inhibitor isoxaben. These results establish a role for IAR4 in the regulation of cell wall function and provide evidence of crosstalk between the cell wall and auxin during cell expansion in the root. Public Library of Science 2014-05-23 /pmc/articles/PMC4032291/ /pubmed/24859261 http://dx.doi.org/10.1371/journal.pone.0098193 Text en © 2014 Steinwand et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Steinwand, Blaire J. Xu, Shouling Polko, Joanna K. Doctor, Stephanie M. Westafer, Mike Kieber, Joseph J. Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title | Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title_full | Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title_fullStr | Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title_full_unstemmed | Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title_short | Alterations in Auxin Homeostasis Suppress Defects in Cell Wall Function |
title_sort | alterations in auxin homeostasis suppress defects in cell wall function |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032291/ https://www.ncbi.nlm.nih.gov/pubmed/24859261 http://dx.doi.org/10.1371/journal.pone.0098193 |
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