Dataset Information

Extensive proteomic approaches to identify glycosylphosphatidylinositol-anchored proteins in Arabidopsis reveal their diverse responses to cold acclimation

ABSTRACT: When plants are exposed to non-freezing low temperatures, they can increase their freezing tolerance (cold acclimation, CA). Changes of plasma membrane (PM) and sterol/sphingolipid-enriched microdomain proteins are thought to be crucial for acquisition of freezing tolerance. Particularly, glycosylphosphatidylinositol-anchored proteins (GPI-APs), which are lipid-modified proteins and potentially targeted to PM surface and apoplast, are deeply-involved in microdomain functions. However, GPI-AP functions in the CA mechanisms are not yet characterized. In present study, we conducted large-scale proteomics to investigate CA-induced GPI-APs in Arabidopsis leaves.

INSTRUMENT(S):

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Leaf

SUBMITTER: Daisuke Takahashi

LAB HEAD: Matsuo Uemura

PROVIDER: PXD002908 | Pride | 2016-07-29

REPOSITORIES: Pride

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Cold acclimation is accompanied by complex responses of glycosylphosphatidylinositol (GPI)-anchored proteins in Arabidopsis.

Takahashi Daisuke D Kawamura Yukio Y Uemura Matsuo M

Journal of experimental botany 20160728 17

Cold acclimation results in changes of the plasma membrane (PM) composition. The PM is considered to contain specific lipid/protein-enriched microdomains which can be extracted as detergent-resistant plasma membrane (DRM). Previous studies in animal cells have demonstrated that glycosylphosphatidylinositol-anchored proteins (GPI-APs) can be targeted to microdomains and/or the apoplast. However, the functional significance of GPI-APs during cold acclimation in plants is not yet fully understood. ...[more]

PMID: 27471282

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Project description:Somatic mutation in the X-linked phosphatidylinositol glycan class A (PIG-A) gene causes glycosylphosphatidylinositol (GPI) anchor deficiency in humans with Paroxysmal Nocturnal Hemoglobinuria (PNH). Clinically, patients with PNH have intravascular hemolysis, venous thrombosis and bone marrow failure. We produced a conditional Pig-a knock-out mouse model specifically inactivating the Pig-a gene in hematopoietic cells to study the role of PIG-A deficiency in PNH pathophysiology. We used Affymetrix Mouse Genome 430 2.0 chips to investigate the gene expression pattern in the mouse model of targeted Pig-a deletion. Experiment Overall Design: We performed microarray analysis on 3 pools of sorted GPI-deficient (GPI-) and GPI normal (GPI+) bone marrow cells derived from the same Pig-a knock-out animals, and identified 1275/669 genes of the 45,101 transcripts potentially available for screening using 2-fold change, <10% false discovery rate (FDR) and percentage of present calls as selection criteria. The major representative genes belong to the category of immune response. We tested whether the molecular differences between GPI- and GPI+ bone marrow cells could be preserved when GPI- cells were transplanted in lethally-irradiated wild type mice (C57BL/6). Microarray analysis was performed using sorted bone marrow cells from 4 animals transplanted with GPI-deficient bone marrow cells (T-GPI-) from Pig-a knock-out donors, 3 animals transplanted with GPI-normal bone marrow cells from C57BL/6 donors (T-GPI+), and GPI-normal bone marrow cells from 4 wild-type C57BL/6 mice (WT-GPI+). We found 296 probesets with 2-fold change cutoff, of which T-GPI- cells had 145 up-regulated genes in comparison to WT-GPI+ cells, and had 123 genes differentially expressed when compared to T-GPI+ cells. The gene expression of the GPI-deficient cells was very similar between the two sets of microarray experiments affirming the maintenance of the phenotype before and after bone marrow cell transplantation.

			Action	DRS
	ApoplastCA01.RAW	Raw
	ApoplastCA02.RAW	Raw
	ApoplastCA03.RAW	Raw
	ApoplastCA04.RAW	Raw
	ApoplastNA01.RAW	Raw