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Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis

The physiological and biochemical mechanisms on boron (B)-induced alleviation of aluminum (B)-toxicity in plants have been examined in some details, but our understanding of the molecular mechanisms underlying these processes is very limited. In this study, we first used the cDNA-AFLP to investigate...

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Autores principales: Zhou, Xin-Xing, Yang, Lin-Tong, Qi, Yi-Ping, Guo, Peng, Chen, Li-Song
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352013/
https://www.ncbi.nlm.nih.gov/pubmed/25747450
http://dx.doi.org/10.1371/journal.pone.0115485
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author Zhou, Xin-Xing
Yang, Lin-Tong
Qi, Yi-Ping
Guo, Peng
Chen, Li-Song
author_facet Zhou, Xin-Xing
Yang, Lin-Tong
Qi, Yi-Ping
Guo, Peng
Chen, Li-Song
author_sort Zhou, Xin-Xing
collection PubMed
description The physiological and biochemical mechanisms on boron (B)-induced alleviation of aluminum (B)-toxicity in plants have been examined in some details, but our understanding of the molecular mechanisms underlying these processes is very limited. In this study, we first used the cDNA-AFLP to investigate the gene expression patterns in Citrus grandis roots responsive to B and Al interactions, and isolated 100 differentially expressed genes. Results showed that genes related to detoxification of reactive oxygen species (ROS) and aldehydes (i.e., glutathione S-transferase zeta class-like isoform X1, thioredoxin M-type 4, and 2-alkenal reductase (NADP(+)-dependent)-like), metabolism (i.e., carboxylesterases and lecithin-cholesterol acyltransferase-like 4-like, nicotianamine aminotransferase A-like isoform X3, thiosulfate sulfurtransferase 18-like isoform X1, and FNR, root isozyme 2), cell transport (i.e., non-specific lipid-transfer protein-like protein At2g13820-like and major facilitator superfamily protein), Ca signal and hormone (i.e., calcium-binding protein CML19-like and IAA-amino acid hydrolase ILR1-like 4-like), gene regulation (i.e., Gag-pol polyprotein) and cell wall modification (i.e., glycosyl hydrolase family 10 protein) might play a role in B-induced alleviation of Al-toxicity. Our results are useful not only for our understanding of molecular processes associated with B-induced alleviation of Al-toxicity, but also for obtaining key molecular genes to enhance Al-tolerance of plants in the future.
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spelling pubmed-43520132015-03-17 Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis Zhou, Xin-Xing Yang, Lin-Tong Qi, Yi-Ping Guo, Peng Chen, Li-Song PLoS One Research Article The physiological and biochemical mechanisms on boron (B)-induced alleviation of aluminum (B)-toxicity in plants have been examined in some details, but our understanding of the molecular mechanisms underlying these processes is very limited. In this study, we first used the cDNA-AFLP to investigate the gene expression patterns in Citrus grandis roots responsive to B and Al interactions, and isolated 100 differentially expressed genes. Results showed that genes related to detoxification of reactive oxygen species (ROS) and aldehydes (i.e., glutathione S-transferase zeta class-like isoform X1, thioredoxin M-type 4, and 2-alkenal reductase (NADP(+)-dependent)-like), metabolism (i.e., carboxylesterases and lecithin-cholesterol acyltransferase-like 4-like, nicotianamine aminotransferase A-like isoform X3, thiosulfate sulfurtransferase 18-like isoform X1, and FNR, root isozyme 2), cell transport (i.e., non-specific lipid-transfer protein-like protein At2g13820-like and major facilitator superfamily protein), Ca signal and hormone (i.e., calcium-binding protein CML19-like and IAA-amino acid hydrolase ILR1-like 4-like), gene regulation (i.e., Gag-pol polyprotein) and cell wall modification (i.e., glycosyl hydrolase family 10 protein) might play a role in B-induced alleviation of Al-toxicity. Our results are useful not only for our understanding of molecular processes associated with B-induced alleviation of Al-toxicity, but also for obtaining key molecular genes to enhance Al-tolerance of plants in the future. Public Library of Science 2015-03-06 /pmc/articles/PMC4352013/ /pubmed/25747450 http://dx.doi.org/10.1371/journal.pone.0115485 Text en © 2015 Zhou 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
Zhou, Xin-Xing
Yang, Lin-Tong
Qi, Yi-Ping
Guo, Peng
Chen, Li-Song
Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title_full Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title_fullStr Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title_full_unstemmed Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title_short Mechanisms on Boron-Induced Alleviation of Aluminum-Toxicity in Citrus grandis Seedlings at a Transcriptional Level Revealed by cDNA-AFLP Analysis
title_sort mechanisms on boron-induced alleviation of aluminum-toxicity in citrus grandis seedlings at a transcriptional level revealed by cdna-aflp analysis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352013/
https://www.ncbi.nlm.nih.gov/pubmed/25747450
http://dx.doi.org/10.1371/journal.pone.0115485
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