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Single cell lineage analysis reveals cell fate determination events during directed β-cell differentiation

ABSTRACT: Single cell lineage analysis reveals cell fate determination events during directed β-cell differentiation

PROVIDER: PRJNA601667 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10902817_1.fastq.gz	Fastqsanger.gz
	SRR10902817_2.fastq.gz	Fastqsanger.gz
	SRR10902818_1.fastq.gz	Fastqsanger.gz
	SRR10902818_2.fastq.gz	Fastqsanger.gz
	SRR10902819_1.fastq.gz	Fastqsanger.gz

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Single cell lineage analysis reveals cell fate determination events during directed β-cell differentiation

Project description:In vitro differentiation of human ES cells into insulin-producing β-like cells offers new opportunities for pancreatic development modeling and potential diabetes therapy. However, the precise molecular events associated with this multi-stage process remain unclear. Here, we generated 95,308 single cell transcriptome data encompassing the entire differentiation process, and reconstructed a tree delineating the fate choices of all major cell populations in both endocrine and non-endocrine lineages. Most detectable genes are dynamically regulated during differentiation, and stage-specific transcription factors create the time-dependent enhancer landscapes. Interestingly, we found that many diabetes/obesity risk genes are only transiently expressed during differentiation. One example is TCF7L2, which peaked during the pancreatic progenitor stages driven by an enhancer located within a diabetes GWAS locus. From the lineage analysis, we found that the NOTCH signaling-downstream gene HES1 is one of the “switch genes” associated with the choice of non-endocrine cell fate; this led to an improved differentiation protocol for better yield of endocrine cells by adjusting the timing of NOTCH inhibition. Additionally, we discovered that ROCKII inhibitor also promotes endocrine differentiation by suppressing non-endocrine lineage. Taken together, our comprehensive single cell lineage analyses provided a valuable resource for the study of pancreatic development and disease etiology.

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Cell fate determination by ubiquitin-dependent regulation of translation

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Cell fate determination by ubiquitin-dependent regulation of ribosome function

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 a human embryonic stem cell model, we identified the vertebrate-specific ubiquitin ligase Cul3KBTBD8 as an essential regulator of neural crest cell formation. Cul3KBTBD8 monoubiquitylates NOLC1 and its paralog TCOF1, whose mutation underlies the developmental disease 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. Affymetrix assays were performed according to the manufacturer's directions on total RNA isolated from three independent samples of human embryonic stem cells (hESC) H1 cells or cells that had been differentiated into embryoid bodies for 6 days. Where indicated, hESC cells were transduced with control shRNA or shRNA targeting KBTBD8 prior to mRNA isolation. HUMAN GENE 1.0 ST ARRAY chips were used.

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