RNA-Seq Reveals Acute Manganese Exposure Increases Endoplasmic Reticulum Related and Lipocalin mRNAs in Caenorhabditis elegans

Martina Rudgalvyte, Juhani Peltonen, Merja Lakso, Richard Nass, Garry Wong

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Manganese (Mn) is an essential nutrient; nonetheless, excessive amounts can accumulate in brain tissues causing manganism, a severe neurological condition. Previous studies have suggested oxidative stress, mitochondria dysfunction, and impaired metabolism pathways as routes for Mn toxicity. Here, we used the nematode Caenorhabditis elegans to analyze gene expression changes after acute Mn exposure using RNA-Seq. L1 stage animals were exposed to 50 mM MnCl2 for 30 min and analyzed at L4. We identified 746 up- and 1828 downregulated genes (FDR corrected p <0.05; two-fold change) that included endoplasmic reticulum related abu and fkb family genes, as well as six of seven lipocalin-related (lpr) family members. These were also verified by qRT-PCR. RNA interference of lpr-5 showed a dramatic increase in whole body vulnerability to Mn exposure. Our studies demonstrate that Mn exposure alters gene transcriptional levels in different cell stress pathways that may ultimately contribute to its toxic effects.

Original languageEnglish (US)
Pages (from-to)97-105
Number of pages9
JournalJournal of Biochemical and Molecular Toxicology
Volume30
Issue number2
DOIs
StatePublished - Feb 1 2016

Fingerprint

Lipocalins
Caenorhabditis elegans
Manganese
Endoplasmic Reticulum
RNA
Messenger RNA
Genes
Mitochondria
Oxidative stress
Poisons
RNA Interference
Metabolism
Gene expression
Nutrients
Toxicity
Brain
Animals
Oxidative Stress
Down-Regulation
Tissue

Keywords

  • Heavy metal
  • Model organism
  • Next-generation sequencing
  • RNAi
  • Transcriptomics

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Molecular Medicine
  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

RNA-Seq Reveals Acute Manganese Exposure Increases Endoplasmic Reticulum Related and Lipocalin mRNAs in Caenorhabditis elegans. / Rudgalvyte, Martina; Peltonen, Juhani; Lakso, Merja; Nass, Richard; Wong, Garry.

In: Journal of Biochemical and Molecular Toxicology, Vol. 30, No. 2, 01.02.2016, p. 97-105.

Research output: Contribution to journalArticle

@article{fde25f9f012e4c75aa2d6330cb58c84c,
title = "RNA-Seq Reveals Acute Manganese Exposure Increases Endoplasmic Reticulum Related and Lipocalin mRNAs in Caenorhabditis elegans",
abstract = "Manganese (Mn) is an essential nutrient; nonetheless, excessive amounts can accumulate in brain tissues causing manganism, a severe neurological condition. Previous studies have suggested oxidative stress, mitochondria dysfunction, and impaired metabolism pathways as routes for Mn toxicity. Here, we used the nematode Caenorhabditis elegans to analyze gene expression changes after acute Mn exposure using RNA-Seq. L1 stage animals were exposed to 50 mM MnCl2 for 30 min and analyzed at L4. We identified 746 up- and 1828 downregulated genes (FDR corrected p <0.05; two-fold change) that included endoplasmic reticulum related abu and fkb family genes, as well as six of seven lipocalin-related (lpr) family members. These were also verified by qRT-PCR. RNA interference of lpr-5 showed a dramatic increase in whole body vulnerability to Mn exposure. Our studies demonstrate that Mn exposure alters gene transcriptional levels in different cell stress pathways that may ultimately contribute to its toxic effects.",
keywords = "Heavy metal, Model organism, Next-generation sequencing, RNAi, Transcriptomics",
author = "Martina Rudgalvyte and Juhani Peltonen and Merja Lakso and Richard Nass and Garry Wong",
year = "2016",
month = "2",
day = "1",
doi = "10.1002/jbt.21768",
language = "English (US)",
volume = "30",
pages = "97--105",
journal = "Journal of Biochemical and Molecular Toxicology",
issn = "1095-6670",
publisher = "John Wiley and Sons Inc.",
number = "2",

}

TY - JOUR

T1 - RNA-Seq Reveals Acute Manganese Exposure Increases Endoplasmic Reticulum Related and Lipocalin mRNAs in Caenorhabditis elegans

AU - Rudgalvyte, Martina

AU - Peltonen, Juhani

AU - Lakso, Merja

AU - Nass, Richard

AU - Wong, Garry

PY - 2016/2/1

Y1 - 2016/2/1

N2 - Manganese (Mn) is an essential nutrient; nonetheless, excessive amounts can accumulate in brain tissues causing manganism, a severe neurological condition. Previous studies have suggested oxidative stress, mitochondria dysfunction, and impaired metabolism pathways as routes for Mn toxicity. Here, we used the nematode Caenorhabditis elegans to analyze gene expression changes after acute Mn exposure using RNA-Seq. L1 stage animals were exposed to 50 mM MnCl2 for 30 min and analyzed at L4. We identified 746 up- and 1828 downregulated genes (FDR corrected p <0.05; two-fold change) that included endoplasmic reticulum related abu and fkb family genes, as well as six of seven lipocalin-related (lpr) family members. These were also verified by qRT-PCR. RNA interference of lpr-5 showed a dramatic increase in whole body vulnerability to Mn exposure. Our studies demonstrate that Mn exposure alters gene transcriptional levels in different cell stress pathways that may ultimately contribute to its toxic effects.

AB - Manganese (Mn) is an essential nutrient; nonetheless, excessive amounts can accumulate in brain tissues causing manganism, a severe neurological condition. Previous studies have suggested oxidative stress, mitochondria dysfunction, and impaired metabolism pathways as routes for Mn toxicity. Here, we used the nematode Caenorhabditis elegans to analyze gene expression changes after acute Mn exposure using RNA-Seq. L1 stage animals were exposed to 50 mM MnCl2 for 30 min and analyzed at L4. We identified 746 up- and 1828 downregulated genes (FDR corrected p <0.05; two-fold change) that included endoplasmic reticulum related abu and fkb family genes, as well as six of seven lipocalin-related (lpr) family members. These were also verified by qRT-PCR. RNA interference of lpr-5 showed a dramatic increase in whole body vulnerability to Mn exposure. Our studies demonstrate that Mn exposure alters gene transcriptional levels in different cell stress pathways that may ultimately contribute to its toxic effects.

KW - Heavy metal

KW - Model organism

KW - Next-generation sequencing

KW - RNAi

KW - Transcriptomics

UR - http://www.scopus.com/inward/record.url?scp=84957839372&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84957839372&partnerID=8YFLogxK

U2 - 10.1002/jbt.21768

DO - 10.1002/jbt.21768

M3 - Article

VL - 30

SP - 97

EP - 105

JO - Journal of Biochemical and Molecular Toxicology

JF - Journal of Biochemical and Molecular Toxicology

SN - 1095-6670

IS - 2

ER -