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The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35

Harmful algal blooms (HABs) cause a variety of deleterious effects on aquatic ecosystems, especially the toxic dinoflagellate Alexandrium tamarense, which poses a serious threat to marine economic and human health based on releasing paralytic shellfish poison into the environment. The algicidal bact...

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Autores principales: Li, Yi, Zhu, Hong, Lei, Xueqian, Zhang, Huajun, Cai, Guanjing, Chen, Zhangran, Fu, Lijun, Xu, Hong, Zheng, Tianling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585090/
https://www.ncbi.nlm.nih.gov/pubmed/26441921
http://dx.doi.org/10.3389/fmicb.2015.00992
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author Li, Yi
Zhu, Hong
Lei, Xueqian
Zhang, Huajun
Cai, Guanjing
Chen, Zhangran
Fu, Lijun
Xu, Hong
Zheng, Tianling
author_facet Li, Yi
Zhu, Hong
Lei, Xueqian
Zhang, Huajun
Cai, Guanjing
Chen, Zhangran
Fu, Lijun
Xu, Hong
Zheng, Tianling
author_sort Li, Yi
collection PubMed
description Harmful algal blooms (HABs) cause a variety of deleterious effects on aquatic ecosystems, especially the toxic dinoflagellate Alexandrium tamarense, which poses a serious threat to marine economic and human health based on releasing paralytic shellfish poison into the environment. The algicidal bacterium Deinococcus sp. Y35 which can induce growth inhibition on A. tamarense was used to investigate the functional mechanism. The growth status, reactive oxygen species (ROS) content, photosynthetic system and the nuclear system of algal cells were determined under algicidal activity. A culture of strain Y35 not only induced overproduction of ROS in algal cells within only 0.5 h of treatment, also decrease the total protein content as well as the response of the antioxidant enzyme. Meanwhile, lipid peroxidation was induced and cell membrane integrity was lost. Photosynthetic pigments including chlorophyll a and carotenoid decreased along with the photosynthetic efficiency being significantly inhibited. At the same time, photosynthesis-related gene expression showed down-regulation. More than, the destruction of cell nuclear structure and inhibition of proliferating cell nuclear antigen (PCNA) related gene expression were confirmed. The potential functional mechanism of the algicidal bacterium on A. tamarense was investigated and provided a novel viewpoint which could be used in HABs control.
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spelling pubmed-45850902015-10-05 The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35 Li, Yi Zhu, Hong Lei, Xueqian Zhang, Huajun Cai, Guanjing Chen, Zhangran Fu, Lijun Xu, Hong Zheng, Tianling Front Microbiol Microbiology Harmful algal blooms (HABs) cause a variety of deleterious effects on aquatic ecosystems, especially the toxic dinoflagellate Alexandrium tamarense, which poses a serious threat to marine economic and human health based on releasing paralytic shellfish poison into the environment. The algicidal bacterium Deinococcus sp. Y35 which can induce growth inhibition on A. tamarense was used to investigate the functional mechanism. The growth status, reactive oxygen species (ROS) content, photosynthetic system and the nuclear system of algal cells were determined under algicidal activity. A culture of strain Y35 not only induced overproduction of ROS in algal cells within only 0.5 h of treatment, also decrease the total protein content as well as the response of the antioxidant enzyme. Meanwhile, lipid peroxidation was induced and cell membrane integrity was lost. Photosynthetic pigments including chlorophyll a and carotenoid decreased along with the photosynthetic efficiency being significantly inhibited. At the same time, photosynthesis-related gene expression showed down-regulation. More than, the destruction of cell nuclear structure and inhibition of proliferating cell nuclear antigen (PCNA) related gene expression were confirmed. The potential functional mechanism of the algicidal bacterium on A. tamarense was investigated and provided a novel viewpoint which could be used in HABs control. Frontiers Media S.A. 2015-09-17 /pmc/articles/PMC4585090/ /pubmed/26441921 http://dx.doi.org/10.3389/fmicb.2015.00992 Text en Copyright © 2015 Li, Zhu, Lei, Zhang, Cai, Chen, Fu, Xu and Zheng. 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) or licensor 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
Li, Yi
Zhu, Hong
Lei, Xueqian
Zhang, Huajun
Cai, Guanjing
Chen, Zhangran
Fu, Lijun
Xu, Hong
Zheng, Tianling
The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title_full The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title_fullStr The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title_full_unstemmed The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title_short The death mechanism of the harmful algal bloom species Alexandrium tamarense induced by algicidal bacterium Deinococcus sp. Y35
title_sort death mechanism of the harmful algal bloom species alexandrium tamarense induced by algicidal bacterium deinococcus sp. y35
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585090/
https://www.ncbi.nlm.nih.gov/pubmed/26441921
http://dx.doi.org/10.3389/fmicb.2015.00992
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