Cell cycle progression is required for nuclear migration of neural progenitor cells

2006 ◽  
Vol 1088 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Masaki Ueno ◽  
Kei-ichi Katayama ◽  
Hirofumi Yamauchi ◽  
Hiroyuki Nakayama ◽  
Kunio Doi
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Neural Progenitor Cells ◽  
Nuclear Migration ◽  
Neural Progenitor ◽  
Cycle Progression

scholarly journals The neurodevelopmental disorder-linked PHF14 complex that forms biomolecular condensates detects DNA damage and promotes repair

2021 ◽  
Author(s):  
Eva-Lotta Käsper ◽  
In-Young Hwang ◽  
Helga Grötsch ◽  
Herman Kar Ho Fung ◽  
Aurélien A. Sérandour ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Neural Progenitor Cells ◽  
Neurodevelopmental Disorder ◽  
Embryonic Stem ◽  
Neural Progenitor ◽  
Cycle Progression

AbstractNumerous chromatin-associated proteins have been linked to neurodevelopmental disorders, yet their molecular functions often remain elusive. PHF14, HMG20A, TCF20 and RAI1 are components of a putative chromatin-associated complex and have been implicated in neurological disorders. Here, we found that Phf14 knockout embryonic stem cells and neural progenitor cells exhibit impaired cell cycle progression and proliferation, inadequate protection of stalled replication forks, and decreased DNA repair. The PHF14 complex rapidly assembles at DNA damage sites and binds to DNA through HMG20A. The PHF14 complex forms DNA-containing phase separated droplets in vitro, where TCF20 facilitates droplet formation. Furthermore, TCF20 maintenance at DNA damage sites is destabilized upon pathological mutation. Our results suggest that the PHF14 complex contributes to DNA damage repair by sensing damaged sites and forming biomolecular condensates, thus supporting cell cycle progression, especially in neural progenitor cells whose spatiotemporal pool is critical for proper brain development.

scholarly journals Comparative Microarray Analysis of Proliferating and Differentiating Murine ENS Progenitor Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Peter Helmut Neckel ◽  
Roland Mohr ◽  
Ying Zhang ◽  
Bernhard Hirt ◽  
Lothar Just
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Developmental Dysplasia ◽  
Cellular Mechanisms ◽  
Differentiation Markers ◽  
Early Differentiation

Postnatal neural progenitor cells of the enteric nervous system are a potential source for future cell replacement therapies of developmental dysplasia like Hirschsprung’s disease. However, little is known about the molecular mechanisms driving the homeostasis and differentiation of this cell pool. In this work, we conducted Affymetrix GeneChip experiments to identify differences in gene regulation between proliferation and early differentiation of enteric neural progenitors from neonatal mice. We detected a total of 1333 regulated genes that were linked to different groups of cellular mechanisms involved in cell cycle, apoptosis, neural proliferation, and differentiation. As expected, we found an augmented inhibition in the gene expression of cell cycle progression as well as an enhanced mRNA expression of neuronal and glial differentiation markers. We further found a marked inactivation of the canonical Wnt pathway after the induction of cellular differentiation. Taken together, these data demonstrate the various molecular mechanisms taking place during the proliferation and early differentiation of enteric neural progenitor cells.

Chemokine receptor CXCR4 signaling modulates the growth factor-induced cell cycle of self-renewing and multipotent neural progenitor cells

Glia ◽  
2010 ◽  
Vol 59 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Meizhang Li ◽  
Cathleen J. Chang ◽  
Justin D. Lathia ◽  
Li Wang ◽  
Holly L. Pacenta ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Progenitor Cells ◽  
Chemokine Receptor ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Cxcr4 Signaling ◽  
Chemokine Receptor Cxcr4

scholarly journals Activation of Evi1 inhibits cell cycle progression and differentiation of hematopoietic progenitor cells

Leukemia ◽  
2012 ◽  
Vol 27 (5) ◽  
pp. 1127-1138 ◽  
Author(s):  
O S Kustikova ◽  
A Schwarzer ◽  
M Stahlhut ◽  
M H Brugman ◽  
T Neumann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Cycle Progression

scholarly journals Nucleophosmin Regulates Cell Cycle Progression and Stress Response in Hematopoietic Stem/Progenitor Cells

2006 ◽  
Vol 281 (24) ◽  
pp. 16536-16545 ◽  
Author(s):  
June Li ◽  
Daniel P. Sejas ◽  
Reena Rani ◽  
Tara Koretsky ◽  
Grover C. Bagby ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stress Response ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Hematopoietic Stem

Nucleophosmin Regulates Differentiation, Cell Cycle Progression, and Stress Response in Hematopoietic Progenitor Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 312-312
Author(s):  
June Li ◽  
Daniel P. Sejas ◽  
Qishen Pang
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Stress Response ◽  
Progenitor Cells ◽  
Cell Cycle Progression ◽  
Proliferative Potential ◽  
Hematopoietic Progenitors ◽  
Cycle Progression ◽  
Hematopoietic Stem ◽  
Empty Vector

Abstract Nucleophosmin (NPM) is a multifunctional protein frequently overexpressed in actively proliferating cells including tumor and hematopoietic stem cells. Strong evidence indicates that NPM is involved in hematopoiesis and leukemic development. Here we report that NPM enhances the proliferative potential of hematopoietic stem/progenitor cells and increases cell survival upon stress challenge. Specifically, lin-Sca1+c-kit+ bone marrow cells transduced with retroviral vector expressing NPM exhibited higher proliferative rates in both short-term liquid culture and clonogenic progenitor cell assays, compared to the cells transduced with empty vector. Interestingly, NPM overexpression appears to inhibit differentiation of myeloid progenitors. Hematopoietic stem/progenitor cells infected with the NPM retrovirus expressed significantly lower levels of mature cell markers Gr-1 and Mac-1 compared to empty vector transduced cells, and majority of the NPM-overexpressing cells remained Sca1+C-Kit+ during the 5-day culture. Bone marrow transplantation experiments demonstrated that NPM overexpression increases long-term multi-lineage repopulating capacity of hematopoietic progenitors. We have not observed any evidence of proliferative disorders or leukemia in recipients transplanted with NPM-expressing progenitors thus far (4 months posttransplantation). Through cell-cycle profile analysis and single-cell division experiments, we showed that NPM overexpression induces rapid entry of hematopoietic progenitors into the cell cycle, probably via promoting G0/G1 to S transition. Furthermore, immunocytochemical and Western-blot analyses demonstrated that NPM-transduced cells expressed higher level of cyclin A compared to vector-transduced cells. Finally, overexpression of NPM significantly increased the survival of hematopoietic progenitors exposed to mitomycin C or hydrogen peroxide, suggesting that NPM can protect cells from DNA damage and oxidative stress. Together, these results indicate that NPM plays an important role in hematopoiesis via mechanisms involving modulation of progenitor differentiation, cell cycle progression, and stress response.

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