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Metabolomics study for investigating the specific role of INOSITOL-REQUIRING ENZYME 1A and INOSITOL-REQUIRING ENZYME 1B under chronic endoplasmic reticulum stress in Arabidopsis thaliana

ABSTRACT:

The Unfolded Protein Response (UPR) is a retrograde, ER-to-nucleus, signalling pathway which is conserved across kingdoms. In plants, it contributes to development, reproduction, immunity and tolerance to abiotic stress. This metabolomic dataset was produced from 14-day-old Arabidopsis thaliana seedlings challenged by tunicamycin (Tm), an antibiotic inhibiting Asn-linked glycosylation in the endoplasmic reticulum (ER), causing an ER stress and eventually activating the UPR. Wild-type (WT), double mutant deficient for two main actors of the UPR (INOSITOL-REQUIRING ENZYME 1A [IRE1A] and INOSITOL-REQUIRING ENZYME 1B [IRE1B]), as well as doubles mutants complemented with either of the WT IRE1 alleles were used as genetic backgrounds in our experimental setup. This allows to distinguish among differentially-overaccumulated metabolites which ones are dependent on IRE1A and/or IRE1B. Also, shoots and roots were harvested separately to determine organ-specific metabolic responses to Tm.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

PROVIDER: MTBLS10609 | MetaboLights | 2024-12-02

REPOSITORIES: MetaboLights

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			Action	DRS
	Blanc_analytique02_ESIneg_01_20068.mzXML	Mzxml
	Blanc_analytique02_ESIneg_01_20124.mzXML	Mzxml
	CQ1_Leaf_ESIneg_01_20069.mzXML	Mzxml
	CQ1_Root_ESIneg_01_20125.mzXML	Mzxml
	CQ2_Leaf_ESIneg_01_20082.mzXML	Mzxml

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Metabolomics study for investigating chronic endoplasmic reticulum stress in Arabidopsis thaliana

Project description:<p>The Unfolded Protein Response (UPR) is a retrograde, ER-to-nucleus, signalling pathway which is conserved across kingdoms. In plants, it contributes to development, reproduction, immunity and tolerance to abiotic stress. This metabolomic dataset was produced from 14-day-old Arabidopsis thaliana seedlings challenged by tunicamycin (Tm), an antibiotic inhibiting Asn-linked glycosylation in the endoplasmic reticulum (ER), causing an ER stress and eventually activating the UPR. Wild-type (WT), bzip60 single mutant and the double mutant deficient for two main actors of the UPR (INOSITOL-REQUIRING ENZYME 1A and INOSITOL-REQUIRING ENZYME 1B) were used as genetic backgrounds in our experimental setup, allowing to distinguish among differentially-overaccumulated metabolites which ones are dependent on IRE1s and/or bZIP60. Also, shoots and roots were harvested separately to determine organ-specific metabolic responses to Tm.</p>

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