Expression data from Arabidopsis gapcp mutant
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE14765 | GEO | 2009/02/10
SECONDARY ACCESSION(S): PRJNA112263
REPOSITORIES: GEO
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Project description:Glycolytic Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) catalyzes the conversion of glyceraldehyde 3-phospate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH. Both cytosolic and plastidial isoforms of GAPDH has been described but the in vivo functions of the plastidial isoforms is unresolved. We generated mutants of the Arabidopsis plastidial GAPDH isoforms (At1g79530, At1g16300; GAPCp1, GAPCp2) and performed a microarray analysis comparing gapcp double (gapcp1 gapcp2) mutant and wild type seedlings Experiment Overall Design: 15-day old Arabidopsis seedlings (Col 0) and gapcp1gapcp2 double mutants were used for RNA extraction and hybridization on Affymetrix microarrays.
2009-02-21 | E-GEOD-14765 | biostudies-arrayexpress
Project description:Glycolytic Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) catalyzes the conversion of glyceraldehyde 3-phospate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH. We generated mutants of the Arabidopsis plastidial GAPDH isoforms (At1g79530, At1g16300; GAPCp1, GAPCp2). gapcp double mutants (gapcp1 gapcp2) display a drastic phenotype of arrested root development and sterility.Complex interactions occurring between ABA and sugar signal transduction pathways have been shown, but the molecular mechanisms connecting both pathways are not well understood. Since we found drastic carbohydrate changes in gapcp1 gapcp2, we studied their response to ABA. by performing a microarray analysis comparing gapcp1 gapcp2 and wild type seedlings after a long term treatment with ABA.
2010-05-11 | GSE21765 | GEO
Project description:Glycolytic Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) catalyzes the conversion of glyceraldehyde 3-phospate to 1,3-bisphosphoglycerate by coupling with the reduction of NAD+ to NADH. We generated mutants of the Arabidopsis plastidial GAPDH isoforms (At1g79530, At1g16300; GAPCp1, GAPCp2). gapcp double mutants (gapcp1 gapcp2) display a drastic phenotype of arrested root development and sterility.Complex interactions occurring between ABA and sugar signal transduction pathways have been shown, but the molecular mechanisms connecting both pathways are not well understood. Since we found drastic carbohydrate changes in gapcp1 gapcp2, we studied their response to ABA. by performing a microarray analysis comparing gapcp1 gapcp2 and wild type seedlings after a long term treatment with ABA. 15-day old Arabidopsis seedlings (Col 0) and gapcp1gapcp2 double mutants were used for RNA extraction and hybridization on Affymetrix microarrays.
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Project description:Hypoxia-inducible factor-1α (HIF1α) attenuates mitochondrial activity while promoting glycolysis. Paradoxically, it remains unknown why lower glycolysis is compromised in human clear cell renal cell carcinomas (ccRCC), in which HIF1α acts a tumor suppressor by inhibiting cell autonomous proliferation. Here we found that unexpectedly, HIF1α suppresses lower glycolysis after the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) step, leading to reduced lactate secretion in different tumor cell types when cells encounter a limited pyruvate supply such as that typically found in the tumor microenvironment in vivo. This is because HIF1α-dependent attenuation of mitochondrial oxygen consumption increases the NADH/NAD+ ratio that suppresses the activity of NADH-sensitive GAPDH glycolytic enzyme. This is manifested when pyruvate supply is limited since pyruvate acts as an electron acceptor that prevents the increment of the NADH/NAD+ ratio. Furthermore, this anti-glycolytic function provides a molecular basis to explain how HIF1α can suppress tumor cell proliferation by increasing the NADH/NAD+ ratio.
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Project description:We previously reported that a recombinant Candida utilis strain expressing a Candida shehatae xylose reductase K275R/N277D, a C. shehatae xylitol dehydrogenase, and xylulokinase from Pichia stipitis produced ethanol from xylose. However, its productivity was low. In this study, metabolomic (CE-TOF MS) and transcriptomic (microarray) analyses were performed to characterize xylose metabolism by the engineered C. utilis and to identify key genetic changes contributing to efficient xylose utilization. Metabolomic analysis revealed that the xylose-fermenting strain accumulated more pentose phosphate pathway intermediates, more NADH, and more glycolytic intermediates upstream of glyceraldehyde 3-phosphate than wild-type. Transcriptomic analysis of the strain grown on xylose indicated a significant increase in expression of genes encoding tricarboxylic acid cycle enzymes, respiratory enzymes, and enzymes involved in ethanol oxidation. To decrease the NADH/NAD+ ratio and increase ethanol yield from the fermentation of xylose, ADH1 encoding NADH-dependent alcohol dehydrogenase was overexpressed. The resultant strain exhibited a 17% increase in ethanol production and a 22% decrease in xylitol accumulation relative to the control.
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Project description:Glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) is emerging as a key player in T-cell development, function and cancer. Here we investigated the role of GAPDH in T-cell development/function by overexpressing GAPDH in the T-cell lineage. Aged mice developed: 1) splenomegaly, 2) enlarged lymph nodes, 3) lymphocyte-infiltrations in the liver and bone marrow. All showed an increase of strongly proliferating and clonal Tfh CXCR5+PD1highCD4+-T cells associated with germinal center B cells and inflammatory cytokine-release. Gene-set-expression-analysis confirmed that this lymphoma was equivalent to human angioimmunoblastic T-cell lymphoma (AITL). Mechanistically, GAPDH induced NF-B pathway in the murine AITL in vivo inhibition of NF-B combined with anti-PD1 increased mice survival and cancer immune response. GAPDH-dependent modulation of NF-B in T-cells allowed to model AITL-disease and evaluate treatments.
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Project description:Glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) is emerging as a key player in T-cell development, function and cancer. Here we investigated the role of GAPDH in T-cell development/function by overexpressing GAPDH in the T-cell lineage. Aged mice developed: 1) splenomegaly, 2) enlarged lymph nodes, 3) lymphocyte-infiltrations in the liver and bone marrow. All showed an increase of strongly proliferating and clonal Tfh CXCR5+PD1highCD4+-T cells associated with germinal center B cells and inflammatory cytokine-release. Gene-set-expression-analysis confirmed that this lymphoma was equivalent to human angioimmunoblastic T-cell lymphoma (AITL). Mechanistically, GAPDH induced NF-kB pathway in the murine AITL in vivo inhibition of NF-kB combined with anti-PD1 increased mice survival and cancer immune response. GAPDH-dependent modulation of NF-kB in T-cells allowed to model AITL-disease and evaluate treatments.
2021-10-20 | GSE121592 | GEO
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