Wnt of the Two Horizons: Putting Stem Cell Self-Renewal and Cell Fate Determination into Context

2014 ◽  
Vol 23 (17) ◽  
pp. 1975-1990 ◽  
Author(s):  
Ryan N. Serio
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Self Renewal ◽  
Fate Determination

scholarly journals Defects in mesenchymal stem cell self-renewal and cell fate determination lead to an osteopenic phenotype in Bmi-1 null mice

2010 ◽  
Vol 25 (3) ◽  
pp. 640-652 ◽  
Author(s):  
Heng-Wei Zhang ◽  
Jiong Ding ◽  
Jian-Liang Jin ◽  
Jian Guo ◽  
Jing-Ning Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Self Renewal ◽  
Fate Determination

Investigation of Hematopoietic Stem Cell and Progenitor Populations: Implication for Cell Fate Determination and Lineage Commitment.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 801-801 ◽  
Author(s):  
Emmanuelle Passegue ◽  
Camilla Forsberg ◽  
Thomas Serwold ◽  
Scott Kogan ◽  
Irving L. Weissman
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Hematopoietic Development ◽  
Fate Determination

Abstract A thorough understanding of the lineage potential of each subset of hematopoietic stem cells (HSC) and progenitor populations is critical to establish an accurate map of cell fate determination during hematopoietic development. A controversy exists whether multipotentiality is conserved until a mutually exclusive segregation of myeloid and lymphoid potentials or whether early progenitor populations sequentially lose lineage potential as they differentiate from the long-term self-renewing HSC (LT-HSC), starting with loss of megakaryocyte/erythrocyte (MegE) potential. Hematopoietic cells at different developmental stages can be prospectively isolated based on a combination of cell surface phenotypes and functional assays in vitro and in vivo. However, assessment of lineage potential of cells other than LT-HSC is complicated by the progressive loss of self-renewal activity in progenitor populations and the lack of congenic surface markers on mature cells of the MegE lineage. Using sensitive in vitro and in vivo approaches, we quantitatively and kinetically assessed the MegE potential of Lineage−/c-Kit+/Sca-1+ (KLS) subsets of mouse bone marrow, including LT-HSC (Thy1.1int/Flk-2−), sort-term HSC (ST-HSCF: Thy1.1int/Flk-2+) and multipotent progenitor population (MPPF: Thy1.1−/Flk-2+), and compared it with the MegE potential of downstream myeloid progenitors (CMP, GMP and MEP) and with their ability to give rise to mature myelomonocytic and lymphoid cells. In contrast to previous reports, we demonstrate that Flk2-positive ST-HSCF and MPPF populations have readily detectable but transient MegE potential in vivo that is more robust than committed myeloid progenitors CMP and MEP. We also show that these cells make clonal colonies in vitro and in vivo in the spleen that contained megakaryocytes and erythrocytes. Moreover, we established the kinetics of mature cell production from each stem and progenitor population, hence providing the timing of these early differentiation events in vivo that is of critical importance when investigating lineage potential. Our results demonstrate that multipotentiality is retained in the KLS “stem cell” fraction of the bone marrow and support a model of hematopoietic development with mutually exclusive segregation of myeloid and lymphoid lineage potential. Taken together with previous findings, they indicate that transition from LT-HSC to ST-HSCF and then to MPPF, is accompanied by progressive lose of self-renewal ability, increased proliferation and change in gene expression programs to prepare multipotent cells to leave the stem cell niche and undergo lineage differentiation. This model is by definition a simplification of a complex biological process but accounts for most, if not all, differentiation events, tolerates plasticity in lineage segregation at early steps of commitment and it accommodates intrinsic lineage preferences during ontogeny and aging.

scholarly journals The Natural and Engineered 3D Microenvironment as a Regulatory Cue During Stem Cell Fate Determination

2009 ◽  
Vol 15 (3) ◽  
pp. 371-380 ◽  
Author(s):  
Amanda W. Lund ◽  
Bülent Yener ◽  
Jan P. Stegemann ◽  
George E. Plopper
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Stem Cell Fate ◽  
Fate Determination ◽  
3D Microenvironment

scholarly journals POGZ controls embryonic stem cell self-renewal and pluripotency by association with esBAF and HP1

2021 ◽  
Author(s):  
Xiaoyun Sun ◽  
Linxi Cheng ◽  
Yuhua Sun
Keyword(s):  
Cell Fate ◽  
Neurodevelopmental Disorders ◽  
Embryonic Stem ◽  
Autism Spectrum ◽  
Specific Gene ◽  
Open Chromatin ◽  
Cell Fate Determination ◽  
Chromatin Remodeler ◽  
Self Renewal ◽  
Fate Determination

AbstractPOGZ, which encodes a multi-domain transcription factor, has been found frequently mutated in neurodevelopmental disorders, particularly autism spectrum disorder (ASD) and intellectual disability (ID). However, little is known about its function in ESC self-renewal and pluripotency, cell fate determination as well as in transcriptional regulation. Here, using embryonic stem cells (ESCs) as model, we show that POGZ plays key roles in the maintenance of ESC and cell fate determination by association with the SWI-SNW chromatin remodeler complex and heterochromatin protein 1 (HP1) proteins. POGZ is essential for the maintenance of ESC undifferentiated state, and loss of POGZ leads to ESC differentiation, likely by up-regulation of primitive endoderm and mesoderm lineage genes and by down-regulation of pluripotency-related genes. Mechanistically, POGZ may control ESC-specific gene expression by association with chromatin remodeler complex esBAF and HP1s, and they can form a PBH triplex. POGZ functions primarily to maintain an open chromatin, as loss of POGZ leads to a reduced chromatin accessibility. Regulation of chromatin under control of POGZ depends on esBAF complex. POGZ is extensively co-localized with OCT4/NANOG genome wide. Taken together, we propose that POGZ is a pluripotency-associated factor, and its absence in ESCs causes failure to maintain a proper ESC-specific chromatin state and transcriptional circuitry of pluripotency, which eventually leads to ESC self-renewal and pluripotency defects. Our work provides important insights into the role of POGZ in ESC self-renewal and pluripotency as well as regulation of transcription, which will be useful for understanding the etiology of neurodevelopmental disorders by POGZ mutation.

Dominant role of the niche in melanocyte stem-cell fate determination

Nature ◽  
2002 ◽  
Vol 416 (6883) ◽  
pp. 854-860 ◽  
Author(s):  
Emi K. Nishimura ◽  
Siobhán A. Jordan ◽  
Hideo Oshima ◽  
Hisahiro Yoshida ◽  
Masatake Osawa ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Dominant Role ◽  
Cell Fate Determination ◽  
Stem Cell Fate ◽  
Fate Determination ◽  
Melanocyte Stem Cell

scholarly journals Discriminating the Independent Influence of Cell Adhesion and Spreading Area on Stem Cell Fate Determination Using Micropatterned Surfaces

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xinlong Wang ◽  
Xiaohong Hu ◽  
Ida Dulińska-Molak ◽  
Naoki Kawazoe ◽  
Yingnan Yang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Adhesion ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Stem Cell Fate ◽  
Spreading Area ◽  
Fate Determination

scholarly journals Stem Cell Fate Determination during Development and Regeneration of Ectodermal Organs

2012 ◽  
Vol 3 ◽  
Author(s):  
Lucía Jiménez-Rojo ◽  
Zoraide Granchi ◽  
Daniel Graf ◽  
Thimios A. Mitsiadis
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Stem Cell Fate ◽  
Fate Determination
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