Increased fitness of pancreatic cancer cells Adapted to nutrient deprivation
Ontology highlight
ABSTRACT: Pancreatic cancer cells adapted to low nutrient conditions share common transcriptional programs that correlate with alterations in open chromatin states.
Project description:We have previously shown that fed-batch processes with the longest uncoupling phase (ethanol adapted) were characterized by induction of storage carbohydrates, a metabolic event typical of yeast cells experiencing nutrient limitation, at the onset of this phase, whereas this metabolic event was not seen in processes with a short uncoupling phase (ethanol non adapted culture). Taken together, our results suggested that reproducible high bioethanol performance in aerated fed-batch process may be linked to the ability of yeast cells to impede ethanol toxicity by triggering a metabolic remodelling reminiscent to that of cells entering a quiescent G0/G1 state. The aim of this study was to search for genes implicated in the induction an ethanol adapted culture vs ethanol non-adapted culture.
Project description:Transcriptional profiling showed that adaptation to nutrient and oxygen deprivation condition is associated with widespread transcriptional reprogramming resulting in the induction of glycolysis and autophagy and repression of the TCA cycle and biosynthesis
Project description:Transcriptional profiling showed that adaptation to nutrient and oxygen deprivation condition is associated with widespread transcriptional reprogramming resulting in the induction of glycolysis and autophagy and repression of the TCA cycle and biosynthesis
Project description:We have previously shown that fed-batch processes with the longest uncoupling phase (ethanol adapted) were characterized by induction of storage carbohydrates, a metabolic event typical of yeast cells experiencing nutrient limitation, at the onset of this phase, whereas this metabolic event was not seen in processes with a short uncoupling phase (ethanol non adapted culture). Taken together, our results suggested that reproducible high bioethanol performance in aerated fed-batch process may be linked to the ability of yeast cells to impede ethanol toxicity by triggering a metabolic remodelling reminiscent to that of cells entering a quiescent G0/G1 state. The aim of this study was to search for genes implicated in the induction an ethanol adapted culture vs ethanol non-adapted culture. We measure the changes in the gene expression of Ethanol adapted culture (Test : fermentation I in ref 17005001[PMID]) and Ethanol non-adapted (reference : Fermentation II in ref 17005001[PMID]) at the same ethanol concentration of 60 g/l and the same growth rate of the cells (0,14 h-1 :Test) and (0,13 h-1 : reference) to reduce the risk of observing secondary effects due to growth and ethanol stress. For each sample, total RNAs from one yeast culture (no biological replicate) were extracted four times (technical replicates -extract). For labelling, we employed a dye-switch (dCTP-Cy3 and dCTP-Cy5) repeated 2 times and hybridized cDNA on four independent microarrays, given rise to eight data value per gene (each gene is duplicate on the slide).
Project description:To thoroughly characterize the diapaused blastocyst induced by ovariectomy, maternal starvation, and nutrient deprivation, we executed RNA-sequencing analyses for ND blastocysts at E4.5, DIA, Sta, K-PC, and K+0.02 blastocysts at E5.5.
Project description:Autophagy is a lysosomal degradation pathway critical for maintaining cellular homeostasis and viability, and is predominantly regarded as a rapid and dynamic cytoplasmic process. To improve our understanding of the transcriptional and epigenetic events associated with autophagy, we performed genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human wildtype and autophagy-deficient cells. We observed that nutrient deprivation leads to the transcriptional induction of numerous autophagy-associated genes. These transcriptional changes are reflected at the epigenetic level (H3K4me3, H3K27ac, and H3K56ac) and are independent of autophagic flux.
Project description:Autophagy is a lysosomal degradation pathway critical for maintaining cellular homeostasis and viability, and is predominantly regarded as a rapid and dynamic cytoplasmic process. To improve our understanding of the transcriptional and epigenetic events associated with autophagy, we performed genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human wildtype and autophagy-deficient cells. We observed that nutrient deprivation leads to the transcriptional induction of numerous autophagy-associated genes. These transcriptional changes are reflected at the epigenetic level (H3K4me3, H3K27ac, and H3K56ac) and are independent of autophagic flux.