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Next Generation Sequencing Facilitates Quantitative Analysis of Hedgehog Signaling Blockade on Macrophage Transcriptomes

ABSTRACT: Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) between macrophages inhibited for Hedgehog signaling and vehicle control.

ORGANISM(S): Mus musculus

PROVIDER: GSE146223 | GEO | 2021/11/10

REPOSITORIES: GEO

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Next Generation Sequencing Facilitates Quantitative Analysis of Hedgehog Signaling Blockade on Macrophage Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Hedgehog Signaling Blockade on Macrophage Transcriptomes

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Next Generation Sequencing Facilitates Quantitative Analysis of Vehicle Control and Vismodegib Treated Tumor Transcriptomes

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Next-generation sequencing facilitates quantitative analysis of wild-type and Nrl(-/-) retinal transcriptomes.

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Next Generation Sequencing Facilitates Quantitative Analysis of Peritoneal Macrophage Transcriptomes

Project description:Purpose:The purpose of this study is to detect activated or silenced genes during KAT8-deficient peritoneal macrophages and the control cells. Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods:Mouse peritoenal macrophages were harvested from mice 3 days after thioglycollate (Merck) injection. Macrophages RNA profiles were generated by deep sequencing,using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation between KAT8-deficient macrophages and the control cells.

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Next Generation Sequencing Facilitates Quantitative Analysis of peritoneal macrophages Transcriptomes of Dnmt3a macrophage conditional knockout mouse

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2016-05-30 | E-GEOD-74750 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Normal Human Kidney Transcriptomes

Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived normal human kidney transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis The kidney tissue was immediately placed and stored in RNAlater® (Ambion), according to the manufacturer’s instruction. The tissue was manually microdissected under microscope in RNAlater® pool for glomerular and tubular compartment. Dissected tissue was homogenized and RNA was prepared using RNAeasy mini columns (Qiagen, Valencia, CA, US), according to the manufacturer’s instructions. RNA quality and quantity were determined using the Laboratory-on-Chip Total RNA PicoKit Agilent BioAnalyzer. Only samples without evidence of degradation were further used (RNA Integrity Number >6).

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Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and EedcKO Forebrain Transcriptomes

Project description:The histone methyltransferase complex PRC2 is a crucial chromatin modifier and controls key steps in developmental transitions and cell fate choices. Mutations in PRC2 core subunits are found in Weaver syndrome with craniofacial defects, intellectual disabilities, and often macrocephaly, but its pathogenicity and molecular mechanism are unknown. Here, we examined the role of PRC2/Eed in neural stem/progenitor cells (NSPCs) during cortical neurogenesis We found that Eed is highly expressed in embryonic cerebral cortex and specific deletion of Eed in forebrain reduced the number of upper layer neurons but not deeper layer neurons and ultimately contributed to abnormal cortical development. In addition, our results revealed that PRC2/Eed regulated Hedgehog signaling pathway through activation of Gli3 not dependent on H3K27me3 but H3K27ac. What?s more, Increased Gli3 in NSPCs could reduce Gli1 expression and contribute to the defects of cortical neurogenesis caused by Eed deletion. Finally, Hedgehog signaling activation with small molecule SAG or genetic inactivation of Ptch1 could partially rescue the cortical neurogenesis defects in vivo after Eed depletion. In general, we identified a novel PRC2/Eed-Gli3-Gli1 regulatory axis that is critical for normal cortical neurogenesis. Our findings define a critical function for PRC2/Eed in cortical development and shed light on the genetic basis of intellectual disabilities of neural developmental disorders caused by PRC2/Eed mutation.

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