Project description:Transformants either containing pCS1 (strain CCS1) or pNIM as control (strain CCS2) were induced by doxycycline (40 ï¾µg/ml) for the indicated times (T0-T10, 0 to 10 min) in hypha-inducing medium (10 % serum, 37 ï¾°C) under a stream of 93.8 % nitrogen, 6 % CO2 and 0.2 % oxygen. For each time point, cDNA of CCS1 and CCS2 were co-hybridised to microarrays and ratios of expression were calculated for each gene. Each gene is represented by duplicate spots on the DNA microarrays.
Project description:Transformants either containing pCS1 (strain CCS1) or pNIM as control (strain CCS2) were induced by doxycycline (40 ï¾µg/ml) for the indicated times (T0-T10, 0 to 10 min) in aerated hypha-inducing medium (10 % serum, 37 ï¾°C). For each time point, cDNA of CCS1 and CCS2 were co-hybridised to microarrays and ratios of expression were calculated for each gene. Each gene is represented by duplicate spots on the DNA microarrays.
Project description:comparison of the transcriptome of Columbia-0 WT and the trienoic fatty acid deficient mutant fad3-2/fad7-2/fad8 in control conditions.
Project description:comparison of the transcriptome of Columbia WT and the jasmonate deficient mutant aos (allene oxide synthase)in control conditions.
Project description:Comparison of wild type and bir6 mutant Arabidopsis thaliana seedlings. The bir6 mutant is resistant to root growth inhibition by buthione sulfoxime, an inhibitor of glutathione biosynthesis.
Project description:Exponentially growing Sulfolobus acidocaldarius were treated with NaAc to generate replication runout and arrest in G2 phase. The cells were then resuspended in fresh acetate-free media which generates a synchronous population. Samples for investigation of gene expression change were taken during the synchronised populations progress through the cell cycle.
Project description:Transcriptional profiling of estrogen regulated genes in human primary osteoblasts. The cells were either treated with estradiol (1 nM) or the pure antagonist ICI 182,780 (Faslodex), which acts as a potent inhibitor of estrogen receptor signaling.
Project description:Chromosomal translocations that fuse the Mixed Lineage Leukemia (MLL) gene with multiple partners typify acute leukemias of infancy as well as therapy-related leukemias. We utilized a conditional knock-in strategy to bypass the embryonic lethality caused by MLL-CBP expression and to assess the immediate effects of induced MLL-CBP expression on hematopoiesis. Within days of activating MLL-CBP, the fusion protein selectively expanded granulocyte/macrophage progenitors (GMP) and enhanced their self-renewal/proliferation. MLL-CBP altered the gene expression program of GMP, upregulating a subset of genes including Hox a9. Inhibition of Hox a9 expression by RNA interference (RNAi) demonstrated that MLL-CBP required Hox a9 for its enhanced cell expansion. Following exposure to sublethal g-irradiation or N-ethyl-N-nitrosourea (ENU), MLL-CBP mice developed myelomonocytic hyperplasia and progressed to fatal myeloproliferative disorders. These represented the spectrum of therapy-induced acute myelomonocytic leukemia (t-AMML)/chronic myelomonocytic leukemia (t-CMML)/myelodysplastic/myeloproliferative disorder (t-MD/MPD) similar to that seen in humans possessing the t(11;16). This model of MLL-CBP therapy-related myeloproliferative disease demonstrates the selectivity of this MLL-fusion for GMP cells and its ability to initiate leukemogenesis in conjunction with cooperating mutations.