Cellular differentiation

About: Cellular differentiation is a research topic. Over the lifetime, 90966 publications have been published within this topic receiving 6099252 citations. The topic is also known as: Cellular differentiation & GO:0030154.

Basal cells as stem cells of the mouse trachea and human airway epithelium

Abstract: The pseudostratified epithelium of the mouse trachea and human airways contains a population of basal cells expressing Trp-63 (p63) and cytokeratins 5 (Krt5) and Krt14. Using a KRT5-CreER(T2) transgenic mouse line for lineage tracing, we show that basal cells generate differentiated cells during postnatal growth and in the adult during both steady state and epithelial repair. We have fractionated mouse basal cells by FACS and identified 627 genes preferentially expressed in a basal subpopulation vs. non-BCs. Analysis reveals potential mechanisms regulating basal cells and allows comparison with other epithelial stem cells. To study basal cell behaviors, we describe a simple in vitro clonal sphere-forming assay in which mouse basal cells self-renew and generate luminal cells, including differentiated ciliated cells, in the absence of stroma. The transcriptional profile identified 2 cell-surface markers, ITGA6 and NGFR, which can be used in combination to purify human lung basal cells by FACS. Like those from the mouse trachea, human airway basal cells both self-renew and generate luminal daughters in the sphere-forming assay.

Memory CD8+ T cell differentiation: initial antigen encounter triggers a developmental program in naïve cells.

Abstract: The rules that govern memory T cell differentiation are not well understood. This study shows that after antigenic stimulation naive CD8+ T cells become committed to dividing at least seven times and differentiating into effector and memory cells. Once the parental naive CD8+ T cell had been activated, this developmental process could not be interrupted and the daughter cells continued to divide and differentiate in the absence of further antigenic stimulation. These data indicate that initial antigen encounter triggers an instructive developmental program that does not require further antigenic stimulation and does not cease until memory CD8+ T cell formation.

Erythroid differentiation in chimaeric mice blocked by a targeted mutation in the gene for transcription factor GATA-1

Abstract: THE zinc-finger transcription factor GATA-1 (previously known as GF-1, NF-E1 or Eryf 1 (refs 1-5)) binds to GATA consensus elements in regulatory regions of theα- and β-globin gene clusters2–6 and other erythroid cell-specific genes7–9. Analysis of the effects of mutations in GATA-binding sites in cell culture and in binding assays in vitro2,5,10,11, as well as transactivation studies with GATA-1 expression vectors in heterologous cells12, have provided indirect evidence that this factor is involved in the activation of globin and other genes during erythroid cell maturation. GATA-1 is also expressed in megakaryocytes13,14 and mast cells13, but not in other blood cell lineages or in non-haemopoietic cells. To investigate the role of this factor in haematopoiesis in vivo. we disrupted the X-linked GATA-1 gene by homologous recombination in a male (XY) murine embryonic stem cell line and tested the GATA-1-deficient cells for their ability to contribute to different tissues in chimaeric mice. The mutant embryonic stem cells contributed to all non-haemopoietic tissues tested and to a white blood cell fraction, but failed to give rise to mature red blood cells. This demonstrates that GATA-1 is required for the normal differentiation of erythroid cells, and that other GATA-binding proteins15,16 cannot compensate for its absence.