scholarly journals Apoptosis in erythroid progenitors deprived of erythropoietin occurs during the G1 and S phases of the cell cycle without growth arrest or stabilization of wild-type p53.

1994 ◽  
Vol 14 (6) ◽  
pp. 4183-4192 ◽  
Author(s):  
L L Kelley ◽  
W F Green ◽  
G G Hicks ◽  
M C Bondurant ◽  
M J Koury ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Conformational Changes ◽  
Dna Analysis ◽  
P53 Protein ◽  
Control Cell ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Wild Type ◽  
Erythroid Progenitors ◽  
Wild Type P53

Erythropoietin (Epo) inhibits apoptosis in murine proerythroblasts infected with the anemia-inducing strain of Friend virus (FVA cells). We have shown that the apoptotic process in FVA cell populations deprived of Epo is asynchronous as a result of a heterogeneity in Epo dependence among individual cells. Here we investigated whether apoptosis in FVA cells correlated with cell cycle phase or stabilization of p53 tumor suppressor protein. DNA analysis in nonapoptotic FVA cell subpopulations cultured without Epo demonstrated little change in the percentages of cells in G1,S, and G2/M phases over time. Analysis of the apoptotic subpopulation revealed high percentages of cells in G1 and S, with few cells in G2/M at any time. When cells were sorted from G1 and S phases prior to culture without Epo, apoptotic cells appeared at the same rate in both populations, indicating that no prior commitment step had occurred in either G1 or S phase. Steady-state wild-type p53 protein levels were very low in FVA cells compared with control cell lines and did not accumulate in Epo-deprived cultures; however, p53 protein did accumulate when FVA cells were treated with the DNA-damaging agent actinomycin D. These data indicate that erythroblast apoptosis caused by Epo deprivation (i) occurs throughout G1 and S phases and does not require cell cycle arrest, (ii) does not have a commitment event related to cell cycle phase, and (iii) is not associated with conformational changes or stabilization of wild-type p53 protein.

Apoptosis in erythroid progenitors deprived of erythropoietin occurs during the G1 and S phases of the cell cycle without growth arrest or stabilization of wild-type p53

1994 ◽  
Vol 14 (6) ◽  
pp. 4183-4192
Author(s):  
L L Kelley ◽  
W F Green ◽  
G G Hicks ◽  
M C Bondurant ◽  
M J Koury ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Conformational Changes ◽  
Dna Analysis ◽  
P53 Protein ◽  
Control Cell ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Wild Type ◽  
Erythroid Progenitors ◽  
Wild Type P53

Erythropoietin (Epo) inhibits apoptosis in murine proerythroblasts infected with the anemia-inducing strain of Friend virus (FVA cells). We have shown that the apoptotic process in FVA cell populations deprived of Epo is asynchronous as a result of a heterogeneity in Epo dependence among individual cells. Here we investigated whether apoptosis in FVA cells correlated with cell cycle phase or stabilization of p53 tumor suppressor protein. DNA analysis in nonapoptotic FVA cell subpopulations cultured without Epo demonstrated little change in the percentages of cells in G1,S, and G2/M phases over time. Analysis of the apoptotic subpopulation revealed high percentages of cells in G1 and S, with few cells in G2/M at any time. When cells were sorted from G1 and S phases prior to culture without Epo, apoptotic cells appeared at the same rate in both populations, indicating that no prior commitment step had occurred in either G1 or S phase. Steady-state wild-type p53 protein levels were very low in FVA cells compared with control cell lines and did not accumulate in Epo-deprived cultures; however, p53 protein did accumulate when FVA cells were treated with the DNA-damaging agent actinomycin D. These data indicate that erythroblast apoptosis caused by Epo deprivation (i) occurs throughout G1 and S phases and does not require cell cycle arrest, (ii) does not have a commitment event related to cell cycle phase, and (iii) is not associated with conformational changes or stabilization of wild-type p53 protein.

scholarly journals Wild-type p53 gene expression induces granulocytic differentiation of HL-60 cells

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2230-2237 ◽  
Author(s):  
S Soddu ◽  
G Blandino ◽  
G Citro ◽  
R Scardigli ◽  
G Piaggio ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cellular Response ◽  
P53 Protein ◽  
Cell Cycle Control ◽  
P53 Gene ◽  
Malignant Cell ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Granulocytic Differentiation ◽  
Wild Type P53

Abstract Overexpression of wild-type p53 gene in malignant cell lines has been shown to inhibit cell proliferation in a number of cases. However, endogenous p53 protein seems to play little role in normal cell-cycle control as suggested by the normal development of p53 null mice, and by the low p53 protein levels expressed in most cell types. Recently, increased expression of endogenous p53 protein has been observed during the cellular response to DNA damage, as well as during differentiation of human hematopoietic cells. To study the role of the p53 gene in hematopoietic differentiation, we introduced the wild-type p53 gene or the temperature-sensitive p53(Val135) mutant into p53-deficient HL-60 promyelocytic leukemia cells. Morphological analysis, flow-cytometric determination of granulocytic or monocytic surface markers, and ability to reduce nitroblue tetrazolium (NBT) demonstrated that expression of exogenous wild-type p53 gene in HL-60 cells induces differentiation through the granulocytic pathway. Proliferation and cell-cycle analysis performed early after expression of wild-type p53 showed that induction of differentiation is not coupled with growth arrest, which suggests that p53 is involved in differentiation independently of its activity on the cell cycle.

scholarly journals Wild-type p53 gene expression induces granulocytic differentiation of HL-60 cells

Blood ◽  
1994 ◽  
Vol 83 (8) ◽  
pp. 2230-2237 ◽  
Author(s):  
S Soddu ◽  
G Blandino ◽  
G Citro ◽  
R Scardigli ◽  
G Piaggio ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cellular Response ◽  
P53 Protein ◽  
Cell Cycle Control ◽  
P53 Gene ◽  
Malignant Cell ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Granulocytic Differentiation ◽  
Wild Type P53

Overexpression of wild-type p53 gene in malignant cell lines has been shown to inhibit cell proliferation in a number of cases. However, endogenous p53 protein seems to play little role in normal cell-cycle control as suggested by the normal development of p53 null mice, and by the low p53 protein levels expressed in most cell types. Recently, increased expression of endogenous p53 protein has been observed during the cellular response to DNA damage, as well as during differentiation of human hematopoietic cells. To study the role of the p53 gene in hematopoietic differentiation, we introduced the wild-type p53 gene or the temperature-sensitive p53(Val135) mutant into p53-deficient HL-60 promyelocytic leukemia cells. Morphological analysis, flow-cytometric determination of granulocytic or monocytic surface markers, and ability to reduce nitroblue tetrazolium (NBT) demonstrated that expression of exogenous wild-type p53 gene in HL-60 cells induces differentiation through the granulocytic pathway. Proliferation and cell-cycle analysis performed early after expression of wild-type p53 showed that induction of differentiation is not coupled with growth arrest, which suggests that p53 is involved in differentiation independently of its activity on the cell cycle.

ABC transporters required for endocytosis and endosomal pH regulation inDictyostelium

2001 ◽  
Vol 114 (21) ◽  
pp. 3923-3932
Author(s):  
Derrick T. Brazill ◽  
Lowell R. Meyer ◽  
R. Diane Hatton ◽  
Debra A. Brock ◽  
Richard H. Gomer
Keyword(s):  
Cell Cycle ◽  
Genetic Interaction ◽  
Ph Regulation ◽  
Physiological State ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Wild Type ◽  
Cell Type ◽  
Initial Cell ◽  
Endosomal Ph

In Dictyostelium, the RtoA protein links both initial cell-type choice and physiological state to cell-cycle phase. rtoA– cells (containing a disruption of the rtoA gene) generally do not develop past the mound stage, and have an abnormal ratio of prestalk and prespore cells. RtoA is also involved in fusion of endocytic/exocytic vesicles. Cells lacking RtoA, although having a normal endocytosis rate, have a decreased exocytosis rate and endosomes with abnormally low pHs. RtoA levels vary during the cell cycle, causing a cell-cycle-dependent modulation of parameters such as cytosolic pH (Brazill et al., 2000). To uncover other genes involved in the RtoA-mediated differentiation, we identified genetic suppressors of rtoA. One of these suppressors disrupted two genes, mdrA1 and mdrA2, a tandem duplication encoding two members of the ATP binding cassette (ABC) transporter superfamily. Disruption of mdrA1/mdrA2 results in release from the developmental block and suppression of the defect in initial cell type choice caused by loss of the rtoA gene. However, this is not accomplished by re-establishing the link between cell type choice and cell cycle phase. MdrA1 protein is localized to the endosome. mdrA1–/mdrA2– cells (containing a disruption of these genes) have an endocytosis rate roughly 70% that of wild-type or rtoA– cells, whereas mdrA1–/mdrA2–/rtoA– cells have an endocytosis rate roughly 20% that of wild-type. The exocytosis rates of mdrA1–/mdrA2– and mdrA1–/mdrA2–/rtoA– are roughly that of wild-type. mdrA1–/mdrA2– endosomes have an unusually high pH, whereas mdrA1–/mdrA2–/rtoA– endosomes have an almost normal pH. The ability of mdrA1/mdrA2 disruption to rescue the cell-type proportion, developmental defects, and endosomal pH defects caused by rtoA disruption, and the ability of rtoA disruption to exacerbate the endocytosis defects caused by mdrA1/mdrA2 disruption, suggest a genetic interaction between rtoA, mdrA1 and mdrA2.

RtoA links initial cell type choice to the cell cycle in Dictyostelium

Development ◽  
1996 ◽  
Vol 122 (11) ◽  
pp. 3677-3685 ◽  
Author(s):  
S.A. Wood ◽  
R.R. Ammann ◽  
D.A. Brock ◽  
L. Li ◽  
T. Spann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Phase ◽  
Cycle Phase ◽  
Wild Type ◽  
Cell Type ◽  
Initial Cell ◽  
M Phase ◽  
In The Wild ◽  
G2 Phase ◽  
Novel Protein

In Dictyostelium, initial cell type choice is correlated with the cell-cycle phase of the cell at the time of starvation. We have isolated a mutant, ratioA (rtoA), with a defect in this mechanism that results in an abnormally high percentage of prestalk cells. The rtoA gene has been cloned and sequenced and codes for a novel protein. The cell cycle is normal in rtoA. In the wild type, prestalk cells differentiate from those cells in S or early G2 phase at starvation and prespore cells from cells in late G2 or M phase at starvation. In rtoA mutants, both prestalk and prespore cells originate randomly from cells in any phase of the cell cycle at starvation.

Growth and cell cycle phase composition of fibroblasts in the reconstituted dermis model.

1990 ◽  
Vol 52 (5) ◽  
pp. 986-992
Author(s):  
Takeshi KONO ◽  
Tsukasa TANII ◽  
Masayoshi FURUKAWA ◽  
Nobuyuki MIZUNO ◽  
Shoji TANIGUCHI ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Phase Composition ◽  
Cell Cycle Phase ◽  
Cycle Phase
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