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Tytuł pozycji:

Molecular response mechanisms of silkworm (Bombyx mori L.) to the toxicity of 1-octyl-3-methylimidazole chloride based on transcriptome analysis of midguts and silk glands.

Tytuł:
Molecular response mechanisms of silkworm (Bombyx mori L.) to the toxicity of 1-octyl-3-methylimidazole chloride based on transcriptome analysis of midguts and silk glands.
Autorzy:
Gao K; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Yang M; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Li B; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Chen R; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Dong J; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Liu Q; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Gao Z; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Guo X; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China.
Deng X; College of Biotechnology, Jiangsu University of Science and Technology, Zhenjiang 212100, People's Republic of China. Electronic address: .
Źródło:
Ecotoxicology and environmental safety [Ecotoxicol Environ Saf] 2021 Dec 20; Vol. 227, pp. 112915. Date of Electronic Publication: 2021 Oct 20.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Amsterdam, Netherlands : Elsevier
MeSH Terms:
Bombyx*/genetics
Animals ; Chlorides ; Gene Expression Profiling ; Silk/genetics ; Transcriptome
Contributed Indexing:
Keywords: 1-octyl-3-methylimidazole chloride; Bombyx mori; Cell apoptosis; Histopathological observation; Molecular mechanism; Transcriptome analysis
Substance Nomenclature:
0 (Chlorides)
0 (Silk)
Entry Date(s):
Date Created: 20211023 Date Completed: 20211110 Latest Revision: 20211110
Update Code:
20240105
DOI:
10.1016/j.ecoenv.2021.112915
PMID:
34687943
Czasopismo naukowe
In a previous study, silkworm larvae were used as a novel model to assess the biotoxicity of ILs, which showed that ILs could cause significant physiological and biochemical changes in midguts and silk glands of the larvae, and result in the death of larvae. In order to investigate the toxicity of 1-octyl-3-methylimidazole chloride ([C 8 mim]Cl) to the larvae at molecular level, RNA-sequencing technology was used to construct transcriptomic profiles of midguts and silk glands in this work. Results showed that a lot of differentially expressed genes (DEGs) were effectively screened out through bioinformatics software based on the transcriptome data and reference genome. To give more detail, 5118 and 2211 DEGs (926 and 822 DEGs) were obtained in the midguts (silk glands) when the larvae were exposed to [C 8 mim]Cl for 6 and 12 h, respectively, relative to the controls. In addition, gene ontology (GO) analysis suggested that the DEGs could be divided into three categories (i.e., biological process, cellular component, and molecular function), and were involved in multiple organelle functions and complex biological processes. Kyoto encyclopedia of genes and genomes (KEGG) analysis showed that the DEGs were enriched in a variety of pathways, such as signal transduction, apoptosis, glycolysis, peroxisome, autophagy, hippo signaling pathway, arginine and proline metabolism. Results of quantitative real-time PCR and histopathological observation indicated that molecular mechanism of the larvae against [C 8 mim]Cl toxicology may be attributed to cell apoptosis regulation via both the mitochondrial pathway and the death receptor-initiated pathway. Thus, these results provided useful data for exploring the toxicity of ILs to insects at molecular level.
(Copyright © 2021. Published by Elsevier Inc.)

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