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:GATA6 is a master regulator of differentiation in the pancreas and its expression levels determine the two main molecular subtypes of pancreatic cancer. High GATA6 contributes to the “classical” pancreatic cancer subtype, which is associated with a higher degree of tumor differentiation and better disease prognosis. However, why GATA6 expression varies across pancreatic cancers and what regulate GATA6 expression remain elusive. Here we report that the oncogenic KRAS-activated ERK signaling suppresses GATA6 transcription in pancreatic cancers. GATA6 mRNA levels inversely correlated with KRAS/ERK activity in pancreatic tumors. A genome-wide CRISPR screen in a GATA6-EGFP reporter knockin cell line identified JUNB as the ERK-regulated transcriptional repressor for GATA6. Active ERK stabilizes JUNB protein while KRAS/ERK inhibition led to ubiquitin-independent proteasomal degradation of JUNB and increased transcription of GATA6. Up-regulation of GATA6 enhanced chemosensitivity of pancreatic cancer cells and KRAS/ERK inhibitors synergized with chemotherapy in a GATA6-dependent manner. Our study identifies how oncogenic KRAS/ERK signaling suppresses GATA6 to cause dedifferentiation in pancreatic cancer. Combining KRAS/ERK inhibitors with standard-of-care chemotherapies could be a promising therapeutic strategy for treating pancreatic cancers.
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: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.