scholarly journals Ectopic Expression of Oct-4 Blocks Progenitor-Cell Differentiation and Causes Dysplasia in Epithelial Tissues

Cell ◽  
2005 ◽  
Vol 121 (3) ◽  
pp. 465-477 ◽  
Author(s):  
Konrad Hochedlinger ◽  
Yasuhiro Yamada ◽  
Caroline Beard ◽  
Rudolf Jaenisch
Keyword(s):  
Cell Differentiation ◽  
Progenitor Cell ◽  
Ectopic Expression ◽  
Epithelial Tissues

scholarly journals METTL3-dependent m6A modification programs T follicular helper cell differentiation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yingpeng Yao ◽  
Ying Yang ◽  
Wenhui Guo ◽  
Lifan Xu ◽  
Menghao You ◽  
...  
Keyword(s):  
T Cells ◽  
Transcriptional Regulation ◽  
Cell Differentiation ◽  
Ectopic Expression ◽  
Signature Genes ◽  
Follicular Helper ◽  
Conditional Deletion ◽  
A Cell ◽  
A Site ◽  
Post Transcriptional Regulation

AbstractT follicular helper (TFH) cells are specialized effector CD4+ T cells critical to humoral immunity. Whether post-transcriptional regulation has a function in TFH cells is unknown. Here, we show conditional deletion of METTL3 (a methyltransferase catalyzing mRNA N6-methyladenosine (m6A) modification) in CD4+ T cells impairs TFH differentiation and germinal center responses in a cell-intrinsic manner in mice. METTL3 is necessary for expression of important TFH signature genes, including Tcf7, Bcl6, Icos and Cxcr5 and these effects depend on intact methyltransferase activity. m6A-miCLIP-seq shows the 3′ UTR of Tcf7 mRNA is subjected to METTL3-dependent m6A modification. Loss of METTL3 or mutation of the Tcf7 3′ UTR m6A site results in accelerated decay of Tcf7 transcripts. Importantly, ectopic expression of TCF-1 (encoded by Tcf7) rectifies TFH defects owing to METTL3 deficiency. Our findings indicate that METTL3 stabilizes Tcf7 transcripts via m6A modification to ensure activation of a TFH transcriptional program, indicating a pivotal function of post-transcriptional regulation in promoting TFH cell differentiation.

scholarly journals Pericytes Stimulate Oligodendrocyte Progenitor Cell Differentiation during CNS Remyelination

Cell Reports ◽  
2017 ◽  
Vol 20 (8) ◽  
pp. 1755-1764 ◽  
Author(s):  
Alerie Guzman De La Fuente ◽  
Simona Lange ◽  
Maria Elena Silva ◽  
Ginez A. Gonzalez ◽  
Herbert Tempfer ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Progenitor Cell ◽  
Oligodendrocyte Progenitor Cell ◽  
Oligodendrocyte Progenitor

scholarly journals Sufu regulation of Hedgehog signaling in P19 cells is required for proper glial cell differentiation

2021 ◽  
Author(s):  
Danielle M. Spice ◽  
Joshua Dierolf ◽  
Gregory M. Kelly
Keyword(s):  
Retinoic Acid ◽  
Cell Differentiation ◽  
Glial Cell ◽  
Neural Differentiation ◽  
Hedgehog Signaling ◽  
Target Genes ◽  
Cell Model ◽  
Ectopic Expression ◽  
Negative Regulator ◽  
Embryonal Carcinoma Cell

AbstractHedgehog signaling is essential for vertebrate development, however, less is known about the negative regulators that influence this pathway during the differentiation of cell fates. Using the mouse P19 embryonal carcinoma cell model, Suppressor of Fused (SUFU), a negative regulator of the Hedgehog pathway, was investigated during retinoic acid-induced neural differentiation. We found Hedgehog signaling was activated in the early phase of neural differentiation and became inactive during terminal differentiation of neurons and astrocytes. SUFU, which regulates signaling at the level of GLI, remained relatively unchanged during the differentiation process, however SUFU loss through CRISPIR-Cas9 gene editing resulted in decreased cell proliferation and ectopic expression of Hedgehog target genes. Interestingly, SUFU-deficient cells were unable to differentiate in the absence of retinoic acid, but when differentiated in its presence they showed delayed and decreased astrocyte differentiation; neuron differentiation did not appear to be affected. Retinoic acid-induced differentiation also caused ectopic activation of Hh target genes in SUFU-deficient cells and while the absence of the GLI3 transcriptional inhibitor suggested the pathway was active, no full-length GLI3 was detected even though the message encoding Gli3 was present. Thus, the study would indicate the proper timing and proportion of glial cell differentiation requires SUFU, and its normal regulation of GLI3 to maintain Hh signaling in an inactive state.

scholarly journals EZH2-dependent chromatin looping controls INK4a and INK4b, but not ARF, during human progenitor cell differentiation and cellular senescence

2009 ◽  
Vol 2 (1) ◽  
pp. 16 ◽  
Author(s):  
Sima Kheradmand Kia ◽  
Parham Solaimani Kartalaei ◽  
Elnaz Farahbakhshian ◽  
Farzin Pourfarzad ◽  
Marieke von Lindern ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Cellular Senescence ◽  
Progenitor Cell ◽  
Chromatin Looping
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