Metabolic activity affects RPE fate during cell reprogramming
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ABSTRACT:
PROVIDER: PRJNA866108 | ENA |
REPOSITORIES: ENA
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Project description:To investigate transcriptomic changes that facilitate the reprogramming of retinal pigment epithelium (RPE) cells to neural retina, chicken RPE explants were cultured for 24 or 48 hours in the presence or absence of the reprogramming factor FGF2. To further interrogate the metabolic requirements of reprogramming, RPE explants were additionally cultured in the presence of the pyruvate dehydrogenase kinase inhibitor dichloroacetate in the presence or absence of FGF2.
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Project description:The plasticity of the retinal pigment epithelium (RPE) has been observed during proliferative vitreoretinopathy (PVR), a defective repair process in humans. In contrast, in the embryonic chick, the RPE can be efficiently reprogrammed to regenerate a complete neural retina after surgical removal and when supplied an exogenous source of FGF2. Here, we analyzed discrete RPE cell populations during early times of transiently reprogrammed (RPE 6 hours post-retinectomy) and reprogrammed (RPE 6 hours post-retinectomy and FGF2 treatment) cells, using laser capture microdissection followed by RNA sequencing (LCM-seq) and computational analysis.
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Project description:Reprogramming to induced pluripotency induces the switch of somatic cell identity to induced pluripotent stem cells (iPSCs). However, the mediators and mechanisms of reprogramming remain largely unclear. To elucidate the mediators and mechanisms of reprogramming, we used a siRNA mediated knockdown approach for selected candidate genes during the conversion of somatic cells into iPSCs. We identified Tox4 as a novel factor that modulates cell fate, using reprogramming efficiency towards iPSCs as an assay. We found that Tox4 is needed early in reprogramming to efficiently generate early reprogramming intermediates, irrespective of reprogramming conditions used. Tox4 enables proper exogenous reprogramming factor expression and the closing and opening of putative somatic and pluripotency enhancers early during reprogramming, respectively. We show that TOX4 protein assembles into a high molecular form. Moreover, Tox4 is also required for the efficient conversion of fibroblasts towards the neuronal fate, suggesting a broader role of Tox4 in modulating cell fate. Our study reveals Tox4 as a novel transcriptional modulator of cell fate that mediates reprogramming from the somatic state to the pluripotent and neuronal fate.
2019-09-19 | GSE127932 | GEO
Project description:Reprogramming to induced pluripotency induces the switch of somatic cell identity to induced pluripotent stem cells (iPSCs). However, the mediators and mechanisms of reprogramming remain largely unclear. To elucidate the mediators and mechanisms of reprogramming, we used a siRNA mediated knockdown approach for selected candidate genes during the conversion of somatic cells into iPSCs. We identified Tox4 as a novel factor that modulates cell fate, using reprogramming efficiency towards iPSCs as an assay. We found that Tox4 is needed early in reprogramming to efficiently generate early reprogramming intermediates, irrespective of reprogramming conditions used. Tox4 enables proper exogenous reprogramming factor expression and the closing and opening of putative somatic and pluripotency enhancers early during reprogramming, respectively. We show that TOX4 protein assembles into a high molecular form. Moreover, Tox4 is also required for the efficient conversion of fibroblasts towards the neuronal fate, suggesting a broader role of Tox4 in modulating cell fate. Our study reveals Tox4 as a novel transcriptional modulator of cell fate that mediates reprogramming from the somatic state to the pluripotent and neuronal fate.
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Project description:Dysfunction of the retinal pigmented epithelium (RPE) results in degeneration of photoreceptors and vision loss and is correlated with common blinding disorders in humans. Although many protein-coding genes are known to be expressed in RPEs and important for their development and maintenance, virtually nothing is known about the in vivo roles of non-protein coding transcripts in RPEs. The expression patterns of microRNAs (miRNAs) have been analyzed in a variety of ocular tissues, and few were implicated to play role in RPE based on studies in cell lines. Herein, through RPE specific conditional mutagenesis of Dicer1 or DGCR8, the importance of miRNA for RPE differentiation was uncovered. Interestingly, miRNAs were found to be dispensable for maintaining the RPE fate and survival, and yet they are essential for acquisition of important RPE properties such as the expression of genes involved in the visual cycle pathway, pigmentation and cell adhesion. Importantly miRNAs of the RPE were found to be required for maturation of the adjacent photoreceptors, specifically for the morphogenesis of the outer segments. The profiles of miRNA and mRNA altered in the Dicer1 deficient RPE point to a key role of miR-204 in regulation of RPE differentiation program in vivo and uncovers the importance of additional novel RPE miRNAs. The study exposes the combined regulatory activity of miRNAs of the RPE, which is required for RPE differentiation and for the development of the adjacent neuroretina. Effect of Dicer 1 deficiency on RPE miRNA and mRNA.
2015-06-16 | E-GEOD-69881 | biostudies-arrayexpress
Project description:Dysfunction of the retinal pigmented epithelium (RPE) results in degeneration of photoreceptors and vision loss and is correlated with common blinding disorders in humans. Although many protein-coding genes are known to be expressed in RPEs and important for their development and maintenance, virtually nothing is known about the in vivo roles of non-protein coding transcripts in RPEs. The expression patterns of microRNAs (miRNAs) have been analyzed in a variety of ocular tissues, and few were implicated to play role in RPE based on studies in cell lines. Herein, through RPE specific conditional mutagenesis of Dicer1 or DGCR8, the importance of miRNA for RPE differentiation was uncovered. Interestingly, miRNAs were found to be dispensable for maintaining the RPE fate and survival, and yet they are essential for acquisition of important RPE properties such as the expression of genes involved in the visual cycle pathway, pigmentation and cell adhesion. Importantly miRNAs of the RPE were found to be required for maturation of the adjacent photoreceptors, specifically for the morphogenesis of the outer segments. The profiles of miRNA and mRNA altered in the Dicer1 deficient RPE point to a key role of miR-204 in regulation of RPE differentiation program in vivo and uncovers the importance of additional novel RPE miRNAs. The study exposes the combined regulatory activity of miRNAs of the RPE, which is required for RPE differentiation and for the development of the adjacent neuroretina. Effect of Dicer 1 deficiency on RPE miRNA and mRNA.
2015-06-16 | E-GEOD-69882 | biostudies-arrayexpress
Project description:Transcriptional Reprogramming during Floral Fate Acquisition
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