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Microcystin-LR - induced changes of hepatopancreatic transcriptome, intenstinal microbiota, and histopatology of freshwater crayfish (Procambarus clarkii). / Zhang, Yu; Li, Zheyu ; Kholodkevich, S.; Sharov, Andrey; Feng, Yujie; Ren, Nanqi; Sun, Kai.

в: Science of the Total Environment, Том 711, 134549, 04.2020.

Результаты исследований: Научные публикации в периодических изданияхстатьяРецензирование

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@article{496c64f34b7d4dff98058bd954420476,
title = "Microcystin-LR - induced changes of hepatopancreatic transcriptome, intenstinal microbiota, and histopatology of freshwater crayfish (Procambarus clarkii)",
abstract = "As a hepatotoxin, microcystin-LR (MC-LR) poses a great threat to aquatic organisms. In this research, the hepatopancreatic transcriptome, intestinal microbiota, and histopathology of Procambarus clarkii (P. clarkii) in response to acute MC-LR exposure were studied. RNA-seq analysis of hepatopancreas identified 372 and 781 differentially expressed genes (DEGs) after treatment with 10 and 40 μg/L MC-LR, respectively. Among the DEGs, 23 genes were immune-related and 21 genes were redox-related. GO functional enrichment analysis revealed that MC-LR could impact nuclear-transcribed mRNA catabolic process, cobalamin- and heme-related processes, and sirohydrochlorin cobaltochelatase activity of P. clarkii. In addition, the only significantly enriched KEGG pathway induced by MC-LR was galactose metabolism pathway. Meanwhile, sequencing of the bacterial 16S rRNA gene demonstrated that MC-LR decreased bacterial richness and diversity, and altered the intestinal microbiota composition. At the phylum level, after 96 h, the abundance of Verrucomicrobia decreased after treatment with 10 and 40 μg/L MC-LR, while Firmicutes increased in the 40 μg/L MC-LR-treated group. At the genus level, the abundances of 15 genera were significantly altered after exposure to MC-LR. Our research demonstrated that MC-LR exposure caused histological alterations such as structural damage of hepatopancreas and intestines. This research provides an insight into the mechanisms associated with MC-LR toxicity in aquatic crustaceans.",
keywords = "crayfish, microcistin, Microcystin-LR, Procambarus clarkii, Hepatopancreatic transcriptome, Intestinal microbiota, Histopathology",
author = "Yu Zhang and Zheyu Li and S. Kholodkevich and Andrey Sharov and Yujie Feng and Nanqi Ren and Kai Sun",
year = "2020",
month = apr,
doi = "10.1016/j.scitotenv.2019.134549",
language = "English",
volume = "711",
journal = "Science of the Total Environment",
issn = "0048-9697",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Microcystin-LR - induced changes of hepatopancreatic transcriptome, intenstinal microbiota, and histopatology of freshwater crayfish (Procambarus clarkii)

AU - Zhang, Yu

AU - Li, Zheyu

AU - Kholodkevich, S.

AU - Sharov, Andrey

AU - Feng, Yujie

AU - Ren, Nanqi

AU - Sun, Kai

PY - 2020/4

Y1 - 2020/4

N2 - As a hepatotoxin, microcystin-LR (MC-LR) poses a great threat to aquatic organisms. In this research, the hepatopancreatic transcriptome, intestinal microbiota, and histopathology of Procambarus clarkii (P. clarkii) in response to acute MC-LR exposure were studied. RNA-seq analysis of hepatopancreas identified 372 and 781 differentially expressed genes (DEGs) after treatment with 10 and 40 μg/L MC-LR, respectively. Among the DEGs, 23 genes were immune-related and 21 genes were redox-related. GO functional enrichment analysis revealed that MC-LR could impact nuclear-transcribed mRNA catabolic process, cobalamin- and heme-related processes, and sirohydrochlorin cobaltochelatase activity of P. clarkii. In addition, the only significantly enriched KEGG pathway induced by MC-LR was galactose metabolism pathway. Meanwhile, sequencing of the bacterial 16S rRNA gene demonstrated that MC-LR decreased bacterial richness and diversity, and altered the intestinal microbiota composition. At the phylum level, after 96 h, the abundance of Verrucomicrobia decreased after treatment with 10 and 40 μg/L MC-LR, while Firmicutes increased in the 40 μg/L MC-LR-treated group. At the genus level, the abundances of 15 genera were significantly altered after exposure to MC-LR. Our research demonstrated that MC-LR exposure caused histological alterations such as structural damage of hepatopancreas and intestines. This research provides an insight into the mechanisms associated with MC-LR toxicity in aquatic crustaceans.

AB - As a hepatotoxin, microcystin-LR (MC-LR) poses a great threat to aquatic organisms. In this research, the hepatopancreatic transcriptome, intestinal microbiota, and histopathology of Procambarus clarkii (P. clarkii) in response to acute MC-LR exposure were studied. RNA-seq analysis of hepatopancreas identified 372 and 781 differentially expressed genes (DEGs) after treatment with 10 and 40 μg/L MC-LR, respectively. Among the DEGs, 23 genes were immune-related and 21 genes were redox-related. GO functional enrichment analysis revealed that MC-LR could impact nuclear-transcribed mRNA catabolic process, cobalamin- and heme-related processes, and sirohydrochlorin cobaltochelatase activity of P. clarkii. In addition, the only significantly enriched KEGG pathway induced by MC-LR was galactose metabolism pathway. Meanwhile, sequencing of the bacterial 16S rRNA gene demonstrated that MC-LR decreased bacterial richness and diversity, and altered the intestinal microbiota composition. At the phylum level, after 96 h, the abundance of Verrucomicrobia decreased after treatment with 10 and 40 μg/L MC-LR, while Firmicutes increased in the 40 μg/L MC-LR-treated group. At the genus level, the abundances of 15 genera were significantly altered after exposure to MC-LR. Our research demonstrated that MC-LR exposure caused histological alterations such as structural damage of hepatopancreas and intestines. This research provides an insight into the mechanisms associated with MC-LR toxicity in aquatic crustaceans.

KW - crayfish, microcistin

KW - Microcystin-LR

KW - Procambarus clarkii

KW - Hepatopancreatic transcriptome

KW - Intestinal microbiota

KW - Histopathology

UR - https://www.sciencedirect.com/science/article/abs/pii/S0048969719345401#!

UR - https://pubmed.ncbi.nlm.nih.gov/31810700/

U2 - 10.1016/j.scitotenv.2019.134549

DO - 10.1016/j.scitotenv.2019.134549

M3 - Article

VL - 711

JO - Science of the Total Environment

JF - Science of the Total Environment

SN - 0048-9697

M1 - 134549

ER -

ID: 49710345