Single-Cell sequence profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE144009 | GEO | 2020/10/19
REPOSITORIES: GEO
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Project description:We sequenced mRNA from cardiomyocytes derived from hESCS in vitro. By using the Cas9n, we generated the QKI null hESCs. The gene expression level and alternative splicing events were compared between 4 control and 4 QkI KO samples. Here, we applied a widely used cardiomyocyte differentiation protocol that was reported to produce a population of more than 90% cardiac troponin T (TNNT2)-positive cardiomyocytes. And we are able to demonstrate that QKI is indespensible to cardiac sarcomerogenesis and cardiac function through its regulation of alternative splicing in genes involved in Z-disc formation, such as ACTN2, NEBL, ABLIM1, and PDLIM5.
2020-10-19 | GSE144008 | GEO
Project description:Single-Cell sequence profile in human cardiomyocytes differentiated from Wt and QKI mutant embryonic stem cells
| PRJNA602493 | ENA
Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.
2016-01-17 | E-MTAB-2375 | biostudies-arrayexpress
Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing. The mRNA profiles of control- and QKI-knockdown BEAS2B cells were generated by deep sequencing using Illumina GAIIx sequencer.
2014-04-14 | E-GEOD-55215 | biostudies-arrayexpress
Project description:QKI is required for myelin formation in the verterbrate brain. It functions by binding RNA and regulating its stability, translation, and/or aternative splicing. We have used Affymetrix exon arrays to assess changes in gene expression in response to QKI knockdown on an exon level in rat CG-4 oligodendrocyte precursor cells. Knockdown cells were compared to control cells. Knockdown groups included QKI siRNA transfection, QKI shRNA stable transfection, and hnRNP A1 transient transfection. Control groups consisted of untransfected, control siRNA transfection, control shRNA stable transfection. Each group was analyzed in triplicate.
2011-01-20 | E-GEOD-26716 | biostudies-arrayexpress
Project description:The first macrophages that seed the developing heart originate from the yolk sac during fetal life. While murine studies reveal important homeostatic and reparative functions in adults, we know little about their roles in the earliest stages of human heart development due to a lack of accessible tissue. Generation of bioengineered human cardiac microtissues from pluripotent stem cells models these first steps in cardiac tissue development, however macrophages have not been included in these studies. To bridge these gaps, we differentiated human embryonic stem cells (hESCs) into primitive LYVE1+ macrophages (hESC-macrophages; akin to yolk sac macrophages) that stably engrafted within cardiac microtissues composed of hESC-cardiomyocytes and fibroblasts to study reciprocal interactions. Engraftment induced a tissue resident macrophage gene program resembling human fetal cardiac macrophages, enriched in efferocytic pathways. Functionally, hESC-macrophages induced production and maturation of cardiomyocyte sarcomeric proteins, and enhanced contractile force, relaxation kinetics, and electrical properties. Mechanistically, the primary effect of hESC-macrophages was during the stressful events surrounding early microtissue formation, where they engaged in phosphatidylserine dependent ingestion of apoptotic cardiomyocyte cargo, which reinforced core resident macrophage identity, reduced microtissue stress and drove hESC-cardiomyocytes to become more similar to human ventricular cardiomyocytes found in early development, both transcriptionally and metabolically. Inhibiting efferocytosis of hESC-cardiomyocytes by hESC-macrophages led to increased cell stress, impaired sarcomeric protein maturation and reduced cardiac microtissue function (contraction and relaxation). Taken together, macrophage-engineered human cardiac microtissues represent a considerably improved model for human heart development, and reveal a major beneficial, yet previously unappreciated role for human primitive macrophages in enhancing cardiac tissue function.
2024-04-03 | PXD050996 | Pride
Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing.
2014-04-14 | GSE55215 | GEO
Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.
2010-05-27 | E-GEOD-21574 | biostudies-arrayexpress
Project description:In CRC cells, lncRNA NONHSAT136151 can bind to protein QKI but does not affect the expression of QKI. The binding of NONHSAT136151 may change the interactino of QKI with its target genes. We used microarrays to detail the abundance of mRNAs enriched by QKI in NONHSAT136151 silenced group and control group in CRC cells.
2023-03-21 | GSE227471 | GEO
Project description:Purpose:RNA_sequencing analysis defined a novel role for the QKI in microglia Methods: microglia mRNA profiles of 4-6 weeks-old wild-type (QKIfl/fl) and microglia specific knockout (QKIfl/fl; cx3r1cre-ert2) mice were generated by Illumina HiSeq 4000 in triplicate. The sequence reads that passed quality filters were trimmed with Trimmomatic v0.39. STAR v2.7.1a was then used to align the reads to the mouse genome (mm10/GRCm38). Gene expression was quantified across all samples with HOMER v4.11.1, and the normalization was carried out through the regularized logarithm (rlog) transformation of DESeq2 v1.26.0. Differential expression between the WT and knockout samples were calculated through DESeq2 v1.26.0, and the gene expression was considered significantly different if the absolute value of the log-fold-change (LFC) was higher than 2, the base means larger than 10 and the false discovery rate (FDR) less than 0.05. Results: RNA-seq data revealed the up-regulation of 326 genes and down-regulation of 294 genes in knockout microglia compare to wt (2-fold change at FDR of 0.05, base mean>10). In particular qkICx3cr1-KO microglia exhibited higher expression of genes that are known to encode proteins related to inflammation (Il-6, Apoe, Cxcl-10, Il-1b, Il-12b, and Tnf). In line with this, functional annotation by DAVID, Reactome and, GO analysis showed enrichment of cell cycle and inflammation-related pathways in the up-regulated transcripts in qkICx3cr1-KO mice. Up-regulated transcripts were further validated using qRT-PCR. Conclusions: Our study represents the first detailed analysis of microglia transcriptomes without QKI expression, with biologic replicates, generated by RNA-seq technology. The data should provide how QKI modulates the microglia gene expression profiles in genome-wide detail.
2020-10-30 | GSE156118 | GEO