scholarly journals Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate

2018 ◽  
Vol 115 (10) ◽  
pp. 2407-2412 ◽  
Author(s):  
Yanjie Wang ◽  
Zan Tang ◽  
Huanwei Huang ◽  
Jiao Li ◽  
Zheng Wang ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Population ◽  
Developmental Plasticity ◽  
Alveolar Type ◽  
Type I ◽  
Rna Seq ◽  
Cell Fates ◽  
Distinct Cell ◽  
Alveolar Surface ◽  
Alveolar Type I Cell

Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air–blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx+Igfbp2+ and Hopx+Igfbp2− AT1 cells, which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx+Igfbp2+ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration.

scholarly journals Expression of histone deacetylase 3 instructs alveolar type I cell differentiation by regulating a Wnt signaling niche in the lung

2016 ◽  
Vol 414 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Xiaoru Wang ◽  
Yi Wang ◽  
Melinda E. Snitow ◽  
Kathleen M. Stewart ◽  
Shanru Li ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Wnt Signaling ◽  
Histone Deacetylase ◽  
Alveolar Type ◽  
Type I ◽  
Histone Deacetylase 3 ◽  
Alveolar Type I Cell

scholarly journals Ras is required for a limited number of cell fates and not for general proliferation in Caenorhabditis elegans.

1997 ◽  
Vol 17 (5) ◽  
pp. 2716-2722 ◽  
Author(s):  
J Yochem ◽  
M Sundaram ◽  
M Han
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Cellular Proliferation ◽  
Duct Cell ◽  
Small Gtpase ◽  
Cell Fates ◽  
Larval Stages ◽  
Culture Cells ◽  
Genetic Mosaic ◽  
Distinct Cell

Experiments with mammalian tissue culture cells have implicated the small GTPase Ras in the control of cellular proliferation. Evidence is presented here that this is not the case for a living animal, the nematode Caenorhabditis elegans: proliferation late in embryogenesis and throughout the four larval stages is not noticeably affected in animals lacking Ras in various parts of their cell lineages. Instead, genetic mosaic analysis of the let-60 gene suggests that Ras is required only, at least later in development (a maternal effect cannot be excluded), for establishment of a few temporally and spatially distinct cell fates. Only one of these, the duct cell fate, appears to be essential for viability.

scholarly journals Unbiased Quantitation of Alveolar Type II to Alveolar Type I Cell Transdifferentiation during Repair after Lung Injury in Mice

2017 ◽  
Vol 57 (5) ◽  
pp. 519-526 ◽  
Author(s):  
Nicole L. Jansing ◽  
Jazalle McClendon ◽  
Peter M. Henson ◽  
Rubin M. Tuder ◽  
Dallas M. Hyde ◽  
...  
Keyword(s):  
Lung Injury ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Cell Transdifferentiation ◽  
Alveolar Type I Cell

scholarly journals The Rho Pathway Mediates Transition to an Alveolar Type I Cell Phenotype During Static Stretch of Alveolar Type II Cells

2010 ◽  
Vol 67 (6) ◽  
pp. 585-590 ◽  
Author(s):  
Cherie D Foster ◽  
Linda S Varghese ◽  
Linda W Gonzales ◽  
Susan S Margulies ◽  
Susan H Guttentag
Keyword(s):  
Cell Phenotype ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Type Ii Cells ◽  
Static Stretch ◽  
Alveolar Type I Cell

scholarly journals On the edge: Evolution of polarity protein BASL and the capacity for stomatal lineage asymmetric divisions

2021 ◽  
Author(s):  
Ido Nir ◽  
Gabriel O Amador ◽  
Yan Gong ◽  
Nicole K Smoot ◽  
Le Cai ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Types ◽  
Cell Fates ◽  
Division Plane ◽  
Asymmetric Cell Divisions ◽  
Cell Divisions ◽  
Distinct Cell ◽  
Asymmetric Divisions ◽  
Stem Cell Divisions ◽  
Stomatal Lineage

Asymmetric and oriented stem cell divisions enable the continued production of patterned tissues. The molecules that guide these divisions include several polarity proteins that are localized to discrete plasma membrane domains, are differentially inherited during asymmetric divisions, and whose scaffolding activities can guide division plane orientation and subsequent cell fates. In the stomatal lineages on the surfaces of plant leaves, asymmetric and oriented divisions create distinct cell types in physiologically optimized patterns. The polarity protein BASL is a major regulator of stomatal lineage division and cell fate asymmetries in Arabidopsis, but its role in the stomatal lineages of other plants was unclear. Here, using phylogenetic and functional assays, we demonstrate that BASL is a dicot specific polarity protein. Among dicots, divergence in BASLs roles may reflect some intrinsic protein differences, but more likely reflects previously unappreciated differences in how asymmetric cell divisions are employed for pattern formation in different species. This multi-species analysis therefore provides insight into the evolution of a unique polarity regulator and into the developmental choices available to cells as they build and pattern tissues.

scholarly journals spalt-dependent switching between two cell fates that are induced by the Drosophila EGF receptor

Development ◽  
2001 ◽  
Vol 128 (5) ◽  
pp. 723-732 ◽  
Author(s):  
P.R. Elstob ◽  
V. Brodu ◽  
A.P. Gould
Keyword(s):  
Cell Fate ◽  
Animal Species ◽  
Egf Receptor ◽  
Zinc Finger Protein ◽  
Cell Types ◽  
Chordotonal Organ ◽  
Egfr Signaling ◽  
Cell Fates ◽  
Finger Protein ◽  
Distinct Cell

Signaling from the EGF receptor (EGFR) can trigger the differentiation of a wide variety of cell types in many animal species. We have explored the mechanisms that generate this diversity using the Drosophila peripheral nervous system. In this context, Spitz (SPI) ligand can induce two alternative cell fates from the dorsolateral ectoderm: chordotonal sensory organs and non-neural oenocytes. We show that the overall number of both cell types that are induced is controlled by the degree of EGFR signaling. In addition, the spalt (sal) gene is identified as a critical component of the oenocyte/chordotonal fate switch. Genetic and expression analyses indicate that the SAL zinc-finger protein promotes oenocyte formation and supresses chordotonal organ induction by acting both downstream and in parallel to the EGFR. To explain these findings, we propose a prime-and-respond model. Here, sal functions prior to signaling as a necessary but not sufficient component of the oenocyte prepattern that also serves to raise the apparent threshold for induction by SPI. Subsequently, sal-dependent SAL upregulation is triggered as part of the oenocyte-specific EGFR response. Thus, a combination of SAL in the responding nucleus and increased SPI ligand production sets the binary cell-fate switch in favour of oenocytes. Together, these studies help to explain how one generic signaling pathway can trigger the differentiation of two distinct cell types.

scholarly journals FateID infers cell fate bias in multipotent progenitors from single-cell RNA-seq data

2017 ◽  
Author(s):  
J.S. Herman ◽  
Sagar ◽  
D. Grün
Keyword(s):  
Single Cell ◽  
Cell Fate ◽  
Learning Algorithm ◽  
Cell Fates ◽  
Lineage Differentiation ◽  
Multipotent Progenitors ◽  
Distinct Cell ◽  
Distinct Lineage ◽  
Cell Transcriptome

Differentiation of multipotent cells is a complex process governed by interactions of thousands of genes subject to substantial expression fluctuations. Resolving cell state heterogeneity arising during this process requires quantification of gene expression within individual cells. However, computational methods linking this heterogeneity to biases towards distinct cell fates are not well established. Here, we perform deep single-cell transcriptome sequencing of ~2,000 bone-marrow derived mouse hematopoietic progenitors enriched for lymphoid lineages. To resolve subtle transcriptome priming indicative of distinct lineage biases, we developed FateID, an iterative supervised learning algorithm for the probabilistic quantification of cell fate bias. FateID delineates domains of fate bias within progenitor populations and permits the derivation of high-resolution differentiation trajectories, revealing a common progenitor population of B cells and plasmacytoid dendritic cells, which we validated by in vitro differentiation assays. We expect that FateID will enhance our understanding of the process of cell fate choice in complex multi-lineage differentiation systems.

scholarly journals Notch and TLR signaling coordinate monocyte cell fate and inflammation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jaba Gamrekelashvili ◽  
Tamar Kapanadze ◽  
Stefan Sablotny ◽  
Corina Ratiu ◽  
Khaled Dastagir ◽  
...  
Keyword(s):  
Cell Fate ◽  
Developmental Plasticity ◽  
Cell Fates ◽  
Tlr Signaling ◽  
Tissue Macrophage ◽  
Inflammatory Conditions ◽  
Conditional Deletion ◽  
Signaling Axis ◽  
Monocyte Cell ◽  
Tlr7 Stimulation

Conventional Ly6Chi monocytes have developmental plasticity for a spectrum of differentiated phagocytes. Here we show, using conditional deletion strategies in a mouse model of Toll-like receptor (TLR) 7-induced inflammation, that the spectrum of developmental cell fates of Ly6Chi monocytes, and the resultant inflammation, is coordinately regulated by TLR and Notch signaling. Cell-intrinsic Notch2 and TLR7-Myd88 pathways independently and synergistically promote Ly6Clo patrolling monocyte development from Ly6Chi monocytes under inflammatory conditions, while impairment in either signaling axis impairs Ly6Clo monocyte development. At the same time, TLR7 stimulation in the absence of functional Notch2 signaling promotes resident tissue macrophage gene expression signatures in monocytes in the blood and ectopic differentiation of Ly6Chi monocytes into macrophages and dendritic cells, which infiltrate the spleen and major blood vessels and are accompanied by aberrant systemic inflammation. Thus, Notch2 is a master regulator of Ly6Chi monocyte cell fate and inflammation in response to TLR signaling.

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