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Transcription profiling of human galactose-1-phosphate uridyltransferase (GALT)-deficient cells reveals novel mechanisms of galactose toxicity

ABSTRACT: Comparison of gene expression profiles in GALT-deficient and GALT-reconstituted cells showed that cells lacking GALT activity responded to galactose challenge by activating a set of genes characteristic of endoplasmic reticulum (ER) stress. This response was specific to galactose insult, as cells grown in glucose or hexose-free media did not exhibit ER stress. Experiment Overall Design: Cells were first grown and then infected in high glucose, then transferred to DMEM, 3 experiments with dye-swap

ORGANISM(S): Homo sapiens

SUBMITTER: Kent Lai

PROVIDER: E-GEOD-4864 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Novel mechanisms of galactose toxicity in human galactose-1-phosphate uridyltransferase (GALT)-deficient cells

Project description:Comparison of gene expression profiles in GALT-deficient and GALT-reconstituted cells showed that cells lacking GALT activity responded to galactose challenge by activating a set of genes characteristic of endoplasmic reticulum (ER) stress. This response was specific to galactose insult, as cells grown in glucose or hexose-free media did not exhibit ER stress. Keywords: GALT infected cells

2007-11-01 | GSE4864 | GEO

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Project description:To better understand the pathophysiology of galactose-1-phosphate uridyltransferase (GALT) deficiency in humans, we studied the mechanisms by which a GALT-deficient yeast survived on galactose medium. Under normal conditions, GALT-deficient yeast cannot grow in medium that contains 0.2% galactose as the sole carbohydrate, a phenotype of Gal(-). We isolated revertants from a GALT-deficient yeast by direct selection for growth in galactose, a phenotype of Gal(+). Comparison of gene expression profiles among wild-type and revertant strains on galactose medium revealed that the revertant down-regulated genes encoding enzymes including galactokinase, galactose permease, and UDP-galactose-4-epimerase (the GAL regulon). By contrast, the revertant strain up-regulated the gene for UDP-glucose pyrophosphorylase, UGP1. There was reduced accumulation of galactose-1-phosphate in the galactose-grown revertant cells when compared to the GALT-deficient parent cells.

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Tiling microarray analysis of gene expression profile of Escherichia coli galT mutant cells under D-galactose-stressed condition

Project description:To understand the altered gene expression by D-galactose in galT cells, the cells were grown in the presence and absence of D-galactose and tiling array analysis was performed for transcriptome profiling. A galT defect causes the disease Galactosemia in human. This work helps us to study the human metabolic disease Galactosemia. Total RNAs were isolated from Escherichia coli galT strain grown in the absence and presence of D-galactose. The transcriptome profile of galT cells was figured out in the galactose-stressed condition.

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Galactose Vs Glucose

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