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Single-Cell Sequencing Analysis of KLF5-Induced Multilineage Reprogramming in EpiSCs

ABSTRACT: Single-Cell Sequencing Analysis of KLF5-Induced Multilineage Reprogramming in EpiSCs

PROVIDER: PRJNA1123589 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR29338305_1.fastq.gz	Fastqsanger.gz
	SRR29338305_2.fastq.gz	Fastqsanger.gz
	SRR29338307_1.fastq.gz	Fastqsanger.gz
	SRR29338307_2.fastq.gz	Fastqsanger.gz

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Single-Cell Sequencing Analysis of KLF5-Induced Multilineage Reprogramming in EpiSCs

Project description:During early embryogenesis, Kruuppel-like factor KLF5 is expressed in inner cell mass (ICM), trophectoderm (TE), and primordial germ cell (PGC). It is wellknow to be essential for specifying the TE fate, as well as redundantly with KLF2/4 for specifying the ICM fate during the first fate segregation. Here, we aimed to clarify whether KLF5 regulates these three fates in vitro. We firstly validated the necessity of KLF5 in mouse trophoblast stem cells (TSCs) and PGC-like cells. Mechanistically, we showed that KLF5 is deeply integrated into the transcriptional networks of ICM, TE and PGC in a context-dependent manner. Furthermore, KLF5 is almost the only factor capable of driving TSC fate from primed epiblast stem cells. It could also induce a transition from the primed to naive state just in the absence of WNT signaling. During this transition, KLF5 generates PGC-like cells, concomitantly. Taken together, our work supports KLF5 as a powerful and versatile specifier in both early embryonic lineage determination and in vitro cell fate reprogramming.

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Klf5 functions as a multi-lineage reprogramming transcription factor

Project description:The transcription factor Klf5 is indispensable for both embryonic (redundantly with Klf4) and extra-embryonic development during pre-implantation, yet its role in re-establishing these different fates in vitro remains largely unexplored. Here, we demonstrate that in the absence of WNT signaling activation at the beginning, ectopic expression of Klf5 in post-implantation epiblast stem cells (EpiSCs) not only induces naïve pluripotency, but also exclusively drives reprogramming into trophoblast stem cells (TSCs) and primordial germ cells (PGCs) by directly reactivating key lineage-specific determinants. Single-cell transcriptome analysis reveals distinct reprogramming trajectories toward these three fates, alongside a non-reprogramming trajectory that driven by Klf5-mediated BMP signaling activation. Moreover, endogenous Klf5 is crucial for establishing TSC and PGC fates from embryonic stem cells driven by other inducers. Our findings highlight Klf5’s multipotent reprogramming capacity and its pivotal role in early TSC and PGC fate specification, offering new insights into its versatile functions during embryonic development.

2025-06-01 | GSE281941 | GEO

Microarray analysis of EpiSCs undergoing reprogramming by Esrrb.

Project description:To characterize the reprogramming of epiblast stem cells (EpiSCs) into embryonic stem cells (ESCs) induced by Esrrb, we performed microarray analysis of Tet-on Esrrb EpiSCs after treatment with doxycycline (Dox).

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ChIP-seq analysis of Esrrb, Nanog, Oct4, and Sox2 in EpiSCs undergoing reprogramming

Project description:To investigate the molecular mechanisms underlying the reprogramming of epiblast stem cells (EpiSCs) into embryonic stem cells (ESCs) induced by Esrrb, we performed ChIP-seq analysis of Esrrb, Nanog, Oct4, and Sox2 in Tet-on Esrrb EpiSCs after treatment with doxycycline (Dox).

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Project description:To examine global gene expression changes during differentiation of epiblast stem cells (EpiSCs) induced by embryoid body (EB) formation, we performed RNA-seq analysis.

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Endogenous Wnt proteins induce differentiation and loss of pluripotency in EpiSCs

Project description:We compared the transcriptomes of EpiSCs maintained in the presence or absence of Wnt pathway inhibitor IWP2. We screened also our gene expression data for potential markers for genuine EpiSCs, maintained in the presence of Wnt inhibition and compared with ESC expression data. We compared the transcriptomes of EpiSCs maintained in the presence or absence of IWP2. The high level of Wnt-induced differentiation occurring in conventional EpiSC cultures may have interfered with the analysis of their characteristics. By applying Wnt inhibitors we are now able to establish the properties of genuine EpiSCs.

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Project description:The objective was to determine the role of Krüppel-like factor 5 (KLF5) in radiation-induced intestinal injury. Mice with intestinal-specific knockdown of KLF5 (Cre+ mice) were generated and their response to radiation was compared with controls (Cre- mice). Mice were given 15 Gy total body irradiation (TBI). The mice intestines were harvested at 6h post TBI and screened for differentially expressed genes by microarray analysis. We identified 11,004 and 2,466 differentially expressed genes in non-irradiated and irradiated mice at 6h post TBI, respectively. KLF5 knockdown down-regulated genes related to DNA damage repair pathways such as nucleotide excision repair, mismatch repair, non-homologous end joining and the Fanconi anemia pathway, which may suggest a novel function of KLF5.

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Bmp4-induced differentiation of EpiSCs depends on Wnt signals

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Etv2-induced MEF reprogramming

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Over-expression and knockdown of KLF5

Project description:Activation of the Ras/Erk pathway upregulates expression of the Kruppel-like Factor 5 (KLF5) transcription factor, and KLF5 is a downstream mediator of Ras oncogenic signaling. Specifically, in bladder and colon cancer cell lines KLF5 upregulates the Ras-pathway target gene cyclin D1, and facilitates entry into the S phase of the cell cycle. Ras mutations are common in lung cancer, but a role for KLF5 in lung tumorigenesis has not been defined. To this end, we manipulated KLF5 expression in four Ras-mutant human lung adenocarcinoma cell lines to find that KLF5 significantly modulates anchorage-independent growth, a mutant Ras phenotype. However, in a mouse model of human lung adenocarcinoma, K-RasG12D does not critically require Klf5 to mediate oncogenesis or induce cyclin D1 expression. Patients with lung tumors expressing high levels of KLF5 have significantly better prognosis than those with low or no KLF5 expression (opposite of mutant Ras prognosis). The latter may be explained by KLF5 transcriptional repression of the ATP-binding cassette, sub-family G (WHITE), member 2 (ABCG2), an anthracycline transporter. In agreement with this, KLF5 knockdown cells display significantly more Hoechst “side population” and resistance to doxorubicin. In summary, while KLF5 is not an obligate partner in Ras oncogenic signaling, KLF5 control of ABCG2 expression is significant to patient survival.

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