Project description:Transcriptome analysis of ESCs treated with a transcription inhibitor, with our without ERK activity to measure Erk-dependent changes in mRNA degradation
Project description:We analyzed the functions of ERK in maternal mRNA degradation in mouse oocytes. By comparing the degradation of transcripts in WT oocytes and KO oocytes, we are able to know the defects in maternal mRNA clearance in ERK-deleted oocytes, and identified the ERK target genes in oocyte maturation.
Project description:We analyzed the functions of BTG family proteins in maternal mRNA degradation in mouse oocytes. By comparing the degradation of transcripts in WT oocytes and KO oocytes, we are able to know the defects in maternal mRNA clearance in BTG4-deleted oocytes, and identified the BTG4 target genes in oocyte cyplasmic maturation. 2 WT oocyte samples at GV stage, 2 WT oocyte samples at MII stage, 2 Btg4-/- oocyte samples at GV stage and 2 Btg4-/- oocyte samples at MII stage?2 WT embryo samples at zygote stage, 2 WT embryo samples at 2-cell stage, 2 Btg4-/- embryo samples at zygote stage and 2 Btg4-/- embryo samples at 2-cell stage , and a WT GV oocyte, a WT MII oocyte, a Erk-/- GV oocyte and a Erk-/- MII oocyte are performed RNA sequencing.
Project description:This SuperSeries is composed of the following subset Series: GSE36341: mRNA degradation in Mycobacterium tuberculosis under aerobic conditions GSE36342: mRNA degradation in Mycobacterium smegmatis under aerobic conditions GSE36343: mRNA degradation in Mycobacterium tuberculosis during cold and hypoxic stress GSE36344: mRNA degradation in Mycobacterium tuberculosis with DosR ectopically induced Refer to individual Series
Project description:Several recent studies, including ours, show that most components of signal transduction cascades including the extracellular signal-regulated protein kinase (ERK), that once were thought to act predominantly in cytoplasm, are in fact recruited to chromatin and are integral components of transcriptional complexes. However, their distribution along whole genome remains uncovered. Here we investigate genome wide recruitment of the ERK pathway components using chromatin immunoprecipitations (ChIP) followed by deep sequencing, ChIP-Seq. Hela-S3 cells were starved for 48 hours (control) and stimulated with EGF at concentration of 100ng/mL for 20 minutes. Cells were fixed with formaldehyde, chromatin isolated and subjected to ChIP reaction. Two technical replicates of ChIP reaction followed by sequencing were performed.
Project description:After induction of DosR from a tet regulated promoter (uninduced controls were treated with an equivalent ammount of the solvent, DMSO), transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0. Three replicates for each condition (DosR induced and uninduced) were sampled after 0, 10, 20, 30, and 60 minutes of mRNA decay for a total of 30 arrays.
Project description:Transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0. Three replicates were sampled before transcription arrest, and after 5 and 10 minutes of mRNA decay for a total of 9 arrays. Five minutes of RNA degradation occurred during the processing of these samples, therefore sample times, indicated in the sample name, represent 0, five, and ten minutes of RNA degradation.
Project description:After induction of DosR from a tet regulated promoter (uninduced controls were treated with an equivalent ammount of the solvent, DMSO), transcription was arrested using 50 ug/ul of rifampin leaving RNA degradation as the sole vector responsible for mRNA abundance. mRNA half-lives were calculated from the decay of signal intensity from T0.
