Project description:Purpose: The goals of this study are to investigate the molecular mechanism by which MEIS1 controls megakaryocytic maturation and thrombopoiesis through compareing the mRNA profiling of Wild Type and MEIS1 deleted H1 drived cells at day6 of megakaryocytic differentiation.
Project description:Purpose: The goals of this study are to investigate the molecular mechanism by which MEIS1 controls HEP specification through compareing the mRNA profiling of Wild Type and MEIS1 deleted H1 drived cells at day3 of hematopoietic differentiation. Conclusions:a large number of genes were down-regulated in MEIS1-deleted H1 hESCs when compared with the wild-type cells. Among those, a number of mammalian hematopoiesis-associated genes such as FLI1, APLN, TAL1 and MYB were significantly down-regulated.
Project description:RNA Sequencing Facilitates Quantitative Analysis of Wild Type and MEIS1 deleted H1 drived cells at day3 of hematopoietic differentiation
Project description:Purpose: The goals of this study are to investigate the molecular mechanism by which MEIS2 controls HEP specification and EHT through compareing the mRNA profiling of Wild Type and MEIS2 deleted H1 drived cells at day4 of hematopoietic differentiation. Methods: mRNA profiles of Wild Type and MEIS2 deleted H1 drived cells at day4 of hematopoietic differentiation were generated by deep sequencing using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Conclusions:a large number of genes were down-regulated in MEIS2-deleted H1 hESCs when compared with the wild-type cells. Among those, a number of mammalian hematopoiesis-associated genes such as TAL1 ,GFI and GATA2 were significantly down-regulated.
Project description:RNA Sequencing Facilitates Quantitative Analysis of Wild Type and MEIS2 deleted H1 drived cells at day4 of hematopoietic differentiation.
Project description:MEIS1 is a transcription factor expressed in hematopoietic stem and progenitor cells (HSPC) and in mature megakaryocytes. In contrast to its role in leukemogenesis, the role of MEIS1 in normal hematopoiesis is largely unknown. We show that MEIS1 can direct human hematopoietic progenitors towards a megakaryocyte-erythroid progenitor (MEP) fate. Ectopoic expression of MEIS1 in CD34+ cells resulted in increased erythroid differentiation at the expense of granulocyte and monocyte (GM) differentiation. MEIS1 overexpression not only skewed differentiation of CMPs towards the erythroid lineage but also reprogrammed GM progenitors towards erythrocyte differentiation. Expression profiling was used to determine the transcriptional changes induced by MEIS1 that lead to the oberved phenotype. A transcriptional program enriched for erythrocytic and megakaryocytic genes was detected.
Project description:The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Our present study suggested it exerts two distinguishable effects in differentiating ES cells. First, it increases the numbers of hematopoietic progenitors and extends their persistence in culture. Second, Meis1 skews hematopoietic differentiation by suppressing erythroid while enhancing megakaryocytic progenitor differentiation. To identify the underlying transcriptional bases of these actions, we carried out microarray analysis to compare the various populations of cells developing in ES differentiation cultures in the presence and absence of Meis1 induction.
Project description:The homeodomain protein Meis1 is essential for definitive hematopoiesis and vascular patterning in the mouse embryo. Meis2, another member of the same family, shares 82% protein identities with Meis1. Our present study suggested Meis2 exerts two distinguishable effects in differentiating ES cells. First, it increases the numbers of hematopoietic progenitors and extends their persistence in culture. Second, Meis2 skews hematopoietic differentiation by suppressing erythroid while enhancing megakaryocytic progenitor differentiation. To identify the underlying transcriptional bases of these actions, we carried out microarray analysis to compare the various populations of cells developing in ES differentiation cultures in the presence and absence of Meis2 induction.