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Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-Seq]

ABSTRACT: Collide-seq: A systematic comparison of how different reprogramming transcription factors achieve conversion as well as an in-depth analysis of how cells resolve the conflict when more than one fate is instructed.

ORGANISM(S): Mus musculus

PROVIDER: GSE211862 | GEO | 2022/09/16

REPOSITORIES: GEO

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Probing cell identity hierarchies by fate titration and collision during direct reprogramming [Cut & Tag]

Project description:Collide-seq: A systematic comparison of how different reprogramming transcription factors achieve conversion as well as an in-depth analysis of how cells resolve the conflict when more than one fate is instructed.

2022-09-16 | GSE210181 | GEO

Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-seq & scATAC-seq]

2022-09-16 | GSE211863 | GEO

Probing cell identity hierarchies by fate titration and collision during direct reprogramming.

Project description:Despite the therapeutic promise of direct reprogramming, basic principles concerning fate erasure and the mechanisms to resolve cell identity conflicts remain unclear. To tackle these fundamental questions, we established a single-cell protocol for the simultaneous analysis of multiple cell fate conversion events based on combinatorial and traceable reprogramming factor expression: Collide-seq. Collide-seq revealed the lack of a common mechanism through which fibroblast-specific gene expression loss is initiated. Moreover, we found that the transcriptome of converting cells abruptly changes when a critical level of each reprogramming factor is attained, with higher or lower levels not contributing to major changes. By simultaneously inducing multiple competing reprogramming factors, we also found a deterministic system, in which titration of fates against each other yields dominant or colliding fates. By investigating one collision in detail, we show that reprogramming factors can disturb cell identity programs independent of their ability to bind their target genes. Taken together, Collide-seq has shed light on several fundamental principles of fate conversion that may aid in improving current reprogramming paradigms.

| S-EPMC9476893 | biostudies-literature

Probing cell identity hierarchies by fate titration and collision during direct reprogramming

Project description:Despite the therapeutic promise of direct reprogramming, basic principles concerning fate erasure and the mechanisms to resolve cell identity conflicts remain unclear. To tackle these fundamental questions, we established a single-cell protocol for the simultaneous analysis of multiple cell fate conversion events based on combinatorial and traceable reprogramming factor expression: Collide-seq. Collide-seq revealed the lack of a common mechanism through which fibroblast specific gene expression loss is initiated. Moreover, we found that the transcriptome of converting cells abruptly changes when a critical level of each reprogramming factor is attained, with higher or lower levels not contributing to major changes. By simultaneously inducing multiple competing reprogramming factors, we also found a deterministic system in which titration of fates against each other yields dominant or colliding fates. By investigating one collision in detail, we show that reprogramming factors can disturb cell identity programs independent of their ability to bind their target genes. Taken together, Collide-seq has shed light on several fundamental principles of fate conversion that may aid improving current reprogramming paradigms.

| S-SCDT-MSB-2022-11129 | biostudies-other

Probing cell identity hierarchies by fate titration and collision during direct reprogramming

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-09-16 | GSE211864 | GEO

Probing cell identity hierarchies by fate titration and collision during direct reprogramming

Project description:Probing cell identity hierarchies by fate titration and collision during direct reprogramming

| PRJNA872397 | ENA

Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-Seq]

Project description:Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-Seq]

| PRJNA872403 | ENA

Probing cell identity hierarchies by fate titration and collision during direct reprogramming [Cut & Tag]

Project description:Probing cell identity hierarchies by fate titration and collision during direct reprogramming [Cut & Tag]

| PRJNA864644 | ENA

Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-seq & scATAC-seq]

Project description:Probing cell identity hierarchies by fate titration and collision during direct reprogramming [scRNA-seq & scATAC-seq]

| PRJNA872404 | ENA

RNA polymerase II collision interrupts convergent transcription (RNA-seq)

Project description:Anti-sense non-coding transcripts, genes-within-genes, and convergent gene pairs are prevalent among eukaryotes. The existence of such transcription units raises the question of what happens when RNA polymerase II (RNAPII) molecules collide head-to-head. Here we use a combination of biochemical and genetic approaches in yeast to show that polymerases transcribing opposite DNA strands cannot bypass each other. RNAPII stops, but does not dissociate upon head-to-head collision in vitro, suggesting that opposing polymerases represent insurmountable obstacles for each other. Head-to-head collision in vivo results in RNAPII stopping as well, and removal of collided RNAPII from the DNA template can be achieved via ubiquitylation-directed proteolysis. Indeed, in cells lacking efficient RNAPII poly-ubiquitylation, the half-life of collided polymerases increases, so that these can be detected between convergent genes by ChIP-Seq. These results provide new insight into fundamental mechanisms of gene traffic control, and point to an unexplored effect of anti-sense transcription on gene regulation via polymerase collision. Total RNA was extracted from WT or Elongin C deletion mutant (elc1M-bM-^HM-^F) cells and strand-specific RNA-Seq was performed. Three biological replicates were performed for WT and elc1M-bM-^HM-^F.

2012-11-30 | E-GEOD-38383 | biostudies-arrayexpress

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