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Serpina3 modulates neuronal cell fate determination (scRNA sequencing)

ABSTRACT: Serpina3 modulates neuronal cell fate determination (scRNA sequencing)

PROVIDER: PRJNA694621 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13520676_1.fastq.gz	Fastqsanger.gz
	SRR13520676_2.fastq.gz	Fastqsanger.gz
	SRR13520677_1.fastq.gz	Fastqsanger.gz
	SRR13520677_2.fastq.gz	Fastqsanger.gz

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Serpina3 modulates neuronal cell fate determination (scRNA sequencing)

Project description:Purpose: To better understand how Serpina3 modulate cortex enpansion and folding. We performed single cell sequencing to reveal the change of cell types in single cell level. Method: Single cell isolation was prepared from P0 telencephalic tissue of wild-type (WT) and serpina3f/+;Nestin-Cre mice. The fragmented cDNAs containing barcode and UMI sequences was built the library. Agilent 2100 Bioanalyzer was used to quality controlled and quantified. Single cell RNA-sequencing analysis was used by the Illumina platform in Annoroad Genomics. Results: Clustering and labeling of these cells visualized on a t-SNE plot between the wild-type (WT) and Serpina3f/+;Nestin-Cre mice brain cortex. Specific layer neurons were increased in Serpina3 knock in mice. Conclusions: Single cell RNA-seq data would provide an overall understanding how SERPINA3 gene contribute to generation of cortical expansion and folding in mice.

2021-01-26 | GSE165440 | GEO

Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum

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Tox4 Modulates Cell Fate Reprogramming

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Tox4 Modulates Cell Fate Reprogramming

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Tox4 Modulates Cell Fate Reprogramming

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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Metabolic determination of cell fate through selective inheritance of mitochondria

Project description:Metabolic characteristics of adult stem cells are distinct from their differentiated progeny, and cellular metabolism is emerging as a potential driver of cell fate conversions. However, how metabolism influences fate determination remains unclear. Here, we identified inherited metabolism imposed by functionally distinct mitochondrial age-classes as a fate determinant in asymmetric division of epithelial stem-like cells. While chronologically old mitochondria support oxidative respiration, new organelles are immature and metabolically less active. Upon cell division, selectively segregated mitochondrial age-classes elicit a metabolic bias in progeny cells, with old mitochondria imposing oxidative energy metabolism inducing differentiation. High pentose phosphate pathway flux, promoting redox maintenance, is favoured in cells receiving newly synthesised mitochondria, and is required to maintain stemness during early fate determination after division. Our results demonstrate that fate decisions are susceptible to intrinsic metabolic bias imposed by selectively inherited mitochondria.

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Dlx1/2-Dependent Expression of Meis2 Promotes Neuronal Fate Determination in the Mammalian Striatum [RNA-seq]

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Cell fate determination by ubiquitin-dependent regulation of translation

Project description:Metazoan development depends on accurate execution of differentiation programs that allow pluripotent stem cells to adopt specific fates. Differentiation is brought about by global changes to chromatin architecture and transcriptional networks, yet whether other regulatory events support cell fate determination is less well understood. Using human embryonic stem cell and Xenopus models, we identified the vertebrate-specific ubiquitin ligase Cul3KBTBD8 as an essential regulator of neural crest specification. Cul3KBTBD8 monoubiquitylates NOLC1 and its paralog TCOF1, whose mutation underlies the craniofacial disorder Treacher Collins Syndrome that is characterized by a loss of cranial neural crest cells. Ubiquitylation of NOLC1 and TCOF1 drives formation of a platform that connects RNA polymerase I with ribosome modification enzymes, thereby altering the translational program of differentiating cells to support the generation of neural crest cells. We conclude that the dynamic regulation of ribosome function is an important feature of cell fate determination. Ribosome profiling and mRNA-Seq

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Translational Landscape in Human Early Neural Fate Determination

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