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
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.
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.
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.
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.
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.