Cytokine induction of proliferation and expression of CDC2 and cyclin a in FDC-P1 myeloid hematopoietic progenitor cells: Regulation of ubiquitous and cell cycle-dependent histone gene transcription factors

1995 ◽  
Vol 59 (3) ◽  
pp. 291-302 ◽  
Author(s):  
A. R. Shakoori ◽  
A. J. van Wijnen ◽  
C. Cooper ◽  
F. Aziz ◽  
M. Birnbaum ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Progenitor Cells ◽  
Gene Transcription ◽  
Histone Gene ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Cytokine Induction ◽  
Cycle Dependent ◽  
Histone Gene Transcription

scholarly journals Histone gene transcription factor binding in extracts of normal human cells.

1991 ◽  
Vol 11 (12) ◽  
pp. 5825-5831 ◽  
Author(s):  
F La Bella ◽  
N Heintz
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Dna Binding ◽  
Gene Transcription ◽  
Binding Activity ◽  
Histone Gene ◽  
Dna Binding Activity ◽  
Normal Human ◽  
Histone Gene Transcription

Transcriptional regulation of mammalian histone genes during S phase is achieved through activation of specific factors which interact with subtype-specific histone gene promoter sequences. It has previously been shown that in HeLa cells this induction is not mediated by obligatory changes in the DNA binding activity of histone gene transcription factors as cells progress through the cell cycle. Recently, it has been reported that the DNA binding properties of a putative histone gene transcription factor may be quite different in normal and transformed cells (J. Holthuis, T. A. Owen, A. J. van Wijnen, K. L. Wright, A. Ramsey-Ewing, M. B. Kennedy, R. Carter, S. C. Cosenza, K. J. Soprano, J. B. Lian, J. L. Stein, and G. S. Stein, Science 247:1454-1457, 1990). To determine whether the properties of well-characterized histone gene transcription factors are altered in transformed versus normal cells, we have examined the DNA binding activity of human histone transcription factors during the WI38 (a primary line of normal human fetal lung fibroblasts) cell cycle. The results demonstrate that the properties of Oct1, H4TF1, and H4TF2 are similar in WI38 and HeLa cells and that their DNA binding activities are constitutive during interphase of both normal and transformed cell lines. Although it remains possible that these factors are directly or indirectly perturbed as a result of cellular transformation, it appears unlikely that transformation results in gross changes in DNA binding activity as cells progress toward division.

Histone gene transcription factor binding in extracts of normal human cells

1991 ◽  
Vol 11 (12) ◽  
pp. 5825-5831
Author(s):  
F La Bella ◽  
N Heintz
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Dna Binding ◽  
Gene Transcription ◽  
Binding Activity ◽  
Histone Gene ◽  
Dna Binding Activity ◽  
Normal Human ◽  
Histone Gene Transcription

Transcriptional regulation of mammalian histone genes during S phase is achieved through activation of specific factors which interact with subtype-specific histone gene promoter sequences. It has previously been shown that in HeLa cells this induction is not mediated by obligatory changes in the DNA binding activity of histone gene transcription factors as cells progress through the cell cycle. Recently, it has been reported that the DNA binding properties of a putative histone gene transcription factor may be quite different in normal and transformed cells (J. Holthuis, T. A. Owen, A. J. van Wijnen, K. L. Wright, A. Ramsey-Ewing, M. B. Kennedy, R. Carter, S. C. Cosenza, K. J. Soprano, J. B. Lian, J. L. Stein, and G. S. Stein, Science 247:1454-1457, 1990). To determine whether the properties of well-characterized histone gene transcription factors are altered in transformed versus normal cells, we have examined the DNA binding activity of human histone transcription factors during the WI38 (a primary line of normal human fetal lung fibroblasts) cell cycle. The results demonstrate that the properties of Oct1, H4TF1, and H4TF2 are similar in WI38 and HeLa cells and that their DNA binding activities are constitutive during interphase of both normal and transformed cell lines. Although it remains possible that these factors are directly or indirectly perturbed as a result of cellular transformation, it appears unlikely that transformation results in gross changes in DNA binding activity as cells progress toward division.

Identification of a new set of cell cycle-regulatory genes that regulate S-phase transcription of histone genes in Saccharomyces cerevisiae

1992 ◽  
Vol 12 (11) ◽  
pp. 5249-5259 ◽  
Author(s):  
H Xu ◽  
U J Kim ◽  
T Schuster ◽  
M Grunstein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Replication ◽  
Gene Transcription ◽  
S Phase ◽  
Histone Gene ◽  
Mrna Synthesis ◽  
Histone Mrna ◽  
Complementation Groups ◽  
Histone Gene Transcription

Histone mRNA synthesis is tightly regulated to S phase of the yeast Saccharomyces cerevisiae cell cycle as a result of transcriptional and posttranscriptional controls. Moreover, histone gene transcription decreases rapidly if DNA replication is inhibited by hydroxyurea or if cells are arrested in G1 by the mating pheromone alpha-factor. To identify the transcriptional controls responsible for cycle-specific histone mRNA synthesis, we have developed a selection for mutations which disrupt this process. Using this approach, we have isolated five mutants (hpc1, hpc2, hpc3, hpc4, and hpc5) in which cell cycle regulation of histone gene transcription is altered. All of these mutations are recessive and belong to separate complementation groups. Of these, only one (hpc1) falls in one of the three complementation groups identified previously by other means (M. A. Osley and D. Lycan, Mol. Cell. Biol. 7:4204-4210, 1987), indicating that at least seven different genes are involved in the cell cycle-specific regulation of histone gene transcription. hpc4 is unique in that derepression occurs only in the presence of hydroxyurea but not alpha-factor, suggesting that at least one of the regulatory factors is specific to histone gene transcription after DNA replication is blocked. One of the hpc mutations (hpc2) suppresses delta insertion mutations in the HIS4 and LYS2 loci. This effect allowed the cloning and sequence analysis of HPC2, which encodes a 67.5-kDa, highly charged basic protein.

scholarly journals Orderly Process of Sequential Cytokine Stimulation Is Required for Activation and Maximal Proliferation of Primitive Human Bone Marrow CD34+ Hematopoietic Progenitor Cells Residing in G0

Blood ◽  
1997 ◽  
Vol 90 (2) ◽  
pp. 658-668 ◽  
Author(s):  
Amy C. Ladd ◽  
Robert Pyatt ◽  
Andre Gothot ◽  
Susan Rice ◽  
Jon McMahel ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Marrow ◽  
Phase I ◽  
Progenitor Cells ◽  
Phase Ii ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Cd34 Cells ◽  
Cytokine Stimulation ◽  
Phase Iv

Abstract Bone marrow (BM) CD34+ cells residing in the G0 phase of cell cycle may be the most suited candidates for the examination of cell cycle activation and proliferation of primitive hematopoietic progenitor cells (HPCs). We designed a double simultaneous labeling technique using both DNA and RNA staining with Hoechst 33342 and Pyronin Y, respectively, to isolate CD34+ cells residing in G0(G0CD34+ ). Using long-term BM cultures and limiting dilution analysis, G0CD34+ cells were found to be enriched for primitive HPCs. In vitro proliferation of G0CD34+ cells in response to sequential cytokine stimulation was examined in a two-step assay. In the first step, cells received a primary stimulation consisting of either stem cell factor (SCF), Flt3-ligand (FL), interleukin-3 (IL-3), or IL-6 for 7 days. In the second step, cells from each group were washed and split into four or more groups, each of which was cultured again for another week with one of the four primary cytokines individually, or in combination. Tracking of progeny cells was accomplished by staining cells with PKH2 on day 0 and with PKH26 on day 7. Overall examination of proliferation patterns over 2 weeks showed that cells could progress into four phases of proliferation. Phase I contained cytokine nonresponsive cells that failed to proliferate. Phase II contained cells dividing up to three times within the first 7 days. Phases III and IV consisted of cells dividing up to five divisions and greater than six divisions, respectively, by the end of the 14-day period. Regardless of the cytokine used for primary stimulation, G0CD34+ cells moved only to phase II by day 7, whereas a substantial percentage of cells incubated with SCF or FL remained in phase I. Cells cultured in SCF or FL for the entire 14-day period did not progress beyond phase III but proliferated into phase IV (with <20% of cells remaining in phases I and II) if IL-3, but not IL-6, was substituted for either cytokine on day 7. G0CD34+ cells incubated with IL-3 for 14 days proliferated the most and progressed into phase IV; however, when SCF was substituted on day 7, cells failed to proliferate into phase IV. Most intriguing was a group of cells, many of which were CD34+, detected in cultures initially stimulated with IL-3, which remained as a distinct population, mostly in G0 /G1 , unable to progress out of phase II regardless of the nature of the second stimulus received on day 7. A small percentage of these cells expressed cyclin E, suggesting that their proliferation arrest may have been mediated by a cyclin-related disruption in cell cycle. These results suggest that a programmed response to sequential cytokine stimulation may be part of a control mechanism required for maintenance of proliferation of primitive HPCs and that unscheduled stimulation of CD34+ cells residing in G0 may result in disruption of cell-cycle regulation.

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 Increased binding and defective migration across fibronectin of cycling hematopoietic progenitor cells

Blood ◽  
2002 ◽  
Vol 99 (6) ◽  
pp. 2023-2031 ◽  
Author(s):  
Olivier Giet ◽  
Dirk R. Van Bockstaele ◽  
Ivano Di Stefano ◽  
Sandra Huygen ◽  
Roland Greimers ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Progenitor Cells ◽  
Bovine Serum ◽  
Binding Capacity ◽  
Hematopoietic Progenitor Cells ◽  
Hematopoietic Progenitor ◽  
Cd34 Cells ◽  
And Migration

Abstract Engraftment of hematopoietic progenitor cells has been shown to decrease during cell cycle transit. We studied cell cycle–associated changes in adhesion and migration of mitotically activated cord blood CD34+ cells. Migration toward medium conditioned by the stromal-derived factor-1–producing cell line MS-5 was studied in bovine serum albumin– and fibronectin (Fn)–coated transwells. Migration was reduced in cycling CD34+ cells and long-term culture-initiating cells (LTC-ICs) compared with their noncycling counterparts across Fn but not across bovine serum albumin. Conversely, Fn binding was higher in cycling CD34+ cells and LTC-ICs compared with noncycling progenitor cells, while adhesion of both subsets to bovine serum albumin was undetectable. The contribution of α4 and α5 integrins in mediating adhesion and migration of activated CD34+ cells onto Fn was analyzed by neutralization experiments. While α4-mediated Fn binding decreased during G2/M, α5 integrin–mediated adhesion increased during transit from G0/G1 to S and G2/M phases. As for migration, the contribution of α4 integrin was similar in all phases, whereas α5-directed migration was lower in G2/M compared with G0/G1and S phases. Defective migration of cycling CD34+ cells was not due to differences in α5 integrin expression. In conclusion, chemotaxis across Fn is less efficient in cycling progenitor cells in correlation with an increased Fn binding capacity. In addition, α4 and α5 integrin functions are independently modulated during cell cycle transit.

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