scholarly journals TrkB/BDNF signaling regulates photoreceptor progenitor cell fate decisions

2006 ◽  
Vol 299 (2) ◽  
pp. 455-465 ◽  
Author(s):  
Brian A. Turner ◽  
Janet Sparrow ◽  
Bolin Cai ◽  
Julie Monroe ◽  
Takashi Mikawa ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Cell Fate Decisions ◽  
Bdnf Signaling

scholarly journals Phosphorylation state of the histone variant H2A.X controls human stem and progenitor cell fate decisions

Cell Reports ◽  
2021 ◽  
Vol 34 (10) ◽  
pp. 108818
Author(s):  
Luca Orlando ◽  
Borko Tanasijevic ◽  
Mio Nakanishi ◽  
Jennifer C. Reid ◽  
Juan L. García-Rodríguez ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Histone Variant ◽  
Phosphorylation State ◽  
Cell Fate Decisions

Extrinsic and intrinsic factors control the genesis of amacrine and cone cells in the rat retina

Development ◽  
1999 ◽  
Vol 126 (3) ◽  
pp. 555-566 ◽  
Author(s):  
M.J. Belliveau ◽  
C.L. Cepko
Keyword(s):  
Progenitor Cells ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Amacrine Cell ◽  
Amacrine Cells ◽  
Environment Change ◽  
Rat Retina ◽  
Cell Fate Decisions ◽  
Cone Cells ◽  
Postnatal Environment

The seven major classes of cells of the vertebrate neural retina are generated from a pool of multipotent progenitor cells. Recent studies suggest a model of retinal development in which both the progenitor cells and the environment change over time (Cepko, C. L., Austin, C. P., Yang, X., Alexiades, M. and Ezzeddine, D. (1996). Proc. Natl. Acad. Sci. USA 93, 589–595). We have utilized a reaggregate culture system to test this model. A labeled population of progenitors from the embryonic rat retina were cultured with an excess of postnatal retinal cells and then assayed for their cell fate choices. We found that the postnatal environment had at least two signals that affected the embryonic cells' choice of fate; one signal inhibited the production of amacrine cells and a second affected the production of cone cells. No increase in cell types generated postnatally was observed. The source of the inhibitor of the amacrine cell fate appeared to be previously generated amacrine cells, suggesting that amacrine cell number is controlled by feedback inhibition. The progenitor cell lost its ability to be inhibited for production of an amacrine cell as it entered M phase of the cell cycle. We suggest that postmitotic cells influence progenitor cell fate decisions, but that they do so in a manner restricted by the intrinsic biases of progenitor cells.

scholarly journals Hyaluronan-Based Three-Dimensional Microenvironment Potently Induces Cardiovascular Progenitor Cell Populations

2013 ◽  
Vol 2013 ◽  
pp. 1-7
Author(s):  
Jessica M. Gluck ◽  
Jennifer Chyu ◽  
Connor Delman ◽  
Sepideh Heydarkhan-Hagvall ◽  
W. Robb MacLellan ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Three Dimensional ◽  
Extrinsic Factors ◽  
Cell Fate Decisions ◽  
3D Microenvironment ◽  
Cell Niche ◽  
The Relationship ◽  
Stem Cell Niches

The relationship between stem cell niches in vivo and their surrounding microenvironment is still relatively unknown. Recent advances have indicated that extrinsic factors within the cardiovascular progenitor cell niche influence maintenance of a multipotent state as well as drive cell-fate decisions. We have previously shown the direct effects of extracellular matrix (ECM) proteins and have now investigated the effects of dimension on the induction of a cardiovascular progenitor cell (CPC) population. We have shown here that the three-dimensionality of a hyaluronan-based hydrogel greatly induces a CPC population, as marked by Flk-1. We have compared the effects of a 3D microenvironment to those of conventional 2D cell culture practices and have found that the 3D microenvironment potently induces a progenitor cell state.

scholarly journals Reconstruction of rat retinal progenitor cell lineages in vitro reveals a surprising degree of stochasticity in cell fate decisions

Development ◽  
2010 ◽  
Vol 138 (2) ◽  
pp. 227-235 ◽  
Author(s):  
F. L. A. F. Gomes ◽  
G. Zhang ◽  
F. Carbonell ◽  
J. A. Correa ◽  
W. A. Harris ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Retinal Progenitor Cell ◽  
Cell Fate Decisions ◽  
Cell Lineages ◽  
Retinal Progenitor

scholarly journals Single cell RNA-seq and ATAC-seq indicate critical roles of Isl1 and Nkx2-5 for cardiac progenitor cell transition states and lineage settlement

2017 ◽  
Author(s):  
Guangshuai Jia ◽  
Jens Preussner ◽  
Stefan Guenther ◽  
Xuejun Yuan ◽  
Michail Yekelchyk ◽  
...  
Keyword(s):  
Single Cell ◽  
Cell Fate ◽  
Regulatory Networks ◽  
Progenitor Cell ◽  
Marker Gene ◽  
Transitional Cell ◽  
Developmental Trajectory ◽  
Open Chromatin ◽  
Cardiac Progenitor Cell ◽  
Cell Fate Decisions

SUMMARYFormation and segregation of cell lineages building the vertebrate heart have been studied extensively by genetic cell tracing techniques and by analysis of single marker gene expression but the underlying gene regulatory networks driving cell fate transitions during early cardiogenesis are only partially understood. Here, we comprehensively characterized mouse cardiac progenitor cells (CPC) marked by Nkx2-5 and Isl1 expression from E7.5 to E9.5 using single-cell RNA sequencing. By leveraging on cell-to-cell heterogeneity, we identified different previously unknown cardiac sub-populations. Reconstruction of the developmental trajectory revealed that Isl1+ CPC represent a transitional cell population maintaining a prolonged multipotent state, whereas extended expression of Nkx2-5 commits CPC to a unidirectional cardiomyocyte fate. Furthermore, we show that CPC fate transitions are associated with distinct open chromatin states, which critically depend on Isl1 and Nkx2-5. Our data provide a model of transcriptional and epigenetic regulations during cardiac progenitor cell fate decisions at single-cell resolution.

scholarly journals Global analysis of proliferation and cell cycle gene expression in the regulation of hematopoietic stem and progenitor cell fates

2005 ◽  
Vol 202 (11) ◽  
pp. 1599-1611 ◽  
Author(s):  
Emmanuelle Passegué ◽  
Amy J. Wagers ◽  
Sylvie Giuriato ◽  
Wade C. Anderson ◽  
Irving L. Weissman
Keyword(s):  
Cell Cycle ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Global Analysis ◽  
Molecular Networks ◽  
Proliferation Index ◽  
Cell Cycle Gene ◽  
Hematopoietic Stem ◽  
Cell Fate Decisions

Knowledge of the molecular networks controlling the proliferation and fate of hematopoietic stem cells (HSC) is essential to understand their function in maintaining blood cell production during normal hematopoiesis and upon clinical transplantation. Using highly purified stem and progenitor cell populations, we define the proliferation index and status of the cell cycle machinery at discrete stages of hematopoietic differentiation and during cytokine-mediated HSC mobilization. We identify distinct sets of cell cycle proteins that specifically associate with differentiation, self-renewal, and maintenance of quiescence in HSC and progenitor cells. Moreover, we describe a striking inequality of function among in vivo cycling and quiescent HSC by demonstrating that their long-term engraftment potential resides predominantly in the G0 fraction. These data provide a direct link between HSC proliferation and function and identify discrete molecular targets in regulating HSC cell fate decisions that could have implications for both the therapeutic use of HSC and the understanding of leukemic transformation.

scholarly journals Human mammary progenitor cell fate decisions are products of interactions with combinatorial microenvironments

2009 ◽  
Vol 1 (1) ◽  
pp. 70-79 ◽  
Author(s):  
Mark A. LaBarge ◽  
Celeste M. Nelson ◽  
Rene Villadsen ◽  
Agla Fridriksdottir ◽  
Jason R. Ruth ◽  
...  
Keyword(s):  
Cell Fate ◽  
Progenitor Cell ◽  
Cell Fate Decisions

scholarly journals Deletion of Mtg16, a Target of t(16;21), Alters Hematopoietic Progenitor Cell Proliferation and Lineage Allocation

2008 ◽  
Vol 28 (20) ◽  
pp. 6234-6247 ◽  
Author(s):  
Brenda J. Chyla ◽  
Isabel Moreno-Miralles ◽  
Melissa A. Steapleton ◽  
Mary Ann Thompson ◽  
Srividya Bhaskara ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cells ◽  
Cell Fate ◽  
Progenitor Cell ◽  
Hematopoietic Progenitor Cell ◽  
Hematopoietic Progenitor ◽  
Erythroid Progenitor ◽  
Cell Fate Decisions ◽  
Erythroid Progenitor Cells ◽  
Progenitor Cell Proliferation

ABSTRACT While a number of DNA binding transcription factors have been identified that control hematopoietic cell fate decisions, only a limited number of transcriptional corepressors (e.g., the retinoblastoma protein [pRB] and the nuclear hormone corepressor [N-CoR]) have been linked to these functions. Here, we show that the transcriptional corepressor Mtg16 (myeloid translocation gene on chromosome 16), which is targeted by t(16;21) in acute myeloid leukemia, is required for hematopoietic progenitor cell fate decisions and for early progenitor cell proliferation. Inactivation of Mtg16 skewed early myeloid progenitor cells toward the granulocytic/macrophage lineage while reducing the numbers of megakaryocyte-erythroid progenitor cells. In addition, inactivation of Mtg16 impaired the rapid expansion of short-term stem cells, multipotent progenitor cells, and megakaryocyte-erythroid progenitor cells that is required under hematopoietic stress/emergency. This impairment appears to be a failure to proliferate rather than an induction of cell death, as expression of c-Myc, but not Bcl2, complemented the Mtg16 − / − defect.

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