Commitment to erythroid differentiation by friend erythroleukemia cells: a stochastic analysis

Gusella, James F.; Geller, Ruth J.; Clarke, Bryan J.; Weeks, Virginia; Housman, David E.

doi:10.1016/0092-8674(76)90113-6

Cited by 351 publications

(185 citation statements)

References 9 publications

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“…These committed cells, which no longer require the presence of the inducing agent to execute the terminal di erentiation and terminal cell division programs, ®rst appear 12 ± 24 h after initiation of inducer treatment, depending on conditions (Gusella et al, 1976). Upon exposure to inducer, the levels of cmyc and c-myb mRNAs decline rapidly and then are reexpressed to nearly preinduction levels at about 24 h, followed by a second decline as cells undergo di erentiation (Lachman and Skoultchi, 1984;Ramsay et al, 1986).…”

Section: Expression Of Pu1 Is Down Regulated As Mel Cells Commit To mentioning

confidence: 99%

Deregulated expression of the PU.1 transcription factor blocks murine erythroleukemia cell terminal differentiation

et al. 1997

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Murine erythroleukemia (MEL) cells are transformed erythroid precursors that are blocked from completing the late stages of erythroid di erentiation. A frequent event in the generation of these malignant cells is deregulation of the hematopoietic-speci®c transcription factor PU.1 (Spi-1) by retroviral insertion of the spleenfocus-forming virus component of Friend virus. During chemically induced reinitiation of MEL cell terminal di erentiation, expression of PU.1 is rapidly downregulated, suggesting that PU.1 might interfere with processes required for terminal di erentiation of erythroid precursors. To investigate the role of PU.1 in erythroid di erentiation we transfected MEL cells with a PU.1 cDNA controlled by the eucaryotic translation elongation factor EF1a promoter. Deregulated expression of PU.1 blocked chemically induced di erentiation and terminal cell division. Deregulated expression of two other protooncogenes, c-myc and c-myb, also has been shown to block MEL di erentiation. We present evidence that PU.1 inhibits terminal di erentiation at an earlier step than c-Myc and c-Myb. Thus reinitiation of MEL cell terminal di erentiation appears to be controlled by an ordered program of turning o several protooncogenes. Down-regulation of PU.1 may be a very early step in this program.

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Section: Expression Of Pu1 Is Down Regulated As Mel Cells Commit To mentioning

confidence: 99%

Deregulated expression of the PU.1 transcription factor blocks murine erythroleukemia cell terminal differentiation

et al. 1997

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“…In addition, cellular DNA undergoes a cyclical change in cytosine methylation (Razin et al 19881. These early events occur at a time when the differentiation process requires the continued presence of inducer, but after 8-12 hr, the cells reach a committed state, in which terminal differentiation continues, and the mouse globin genes are expressed in the absence of inducer {Gusella et al 1976;Chen et al 1982).…”

mentioning

confidence: 99%

Induction by HMBA and DMSO of genes introduced into mouse erythroleukemia and other cell lines by transient transfection.

Campbell

Kulozik²,

Woodham³

1990

Genes Dev.

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We have found rapid induction of various genes, including human globin genes, in response to hexamethylene bisacetamide (HMBA) and dimethyl sulfoxide (DMSO) in transiently transfected cells. In mouse erythroleukemia cells (MELCs), this effect is detected within 1 hr of exposure of the cells to inducer before the endogenous mouse globin genes are induced. It does not require protein synthesis and is reversed if the inducer is removed. This and other evidence suggest that the mechanism involves a change in activity of a factor intimately involved with transcription, probably as a result of post-translational modification. As such, it may represent an early triggering event in terminal differentiation, and its relevance to the expression of human globin genes in stable transfectants and to induction of the mouse globin genes is discussed. Other cell lines (K562 and NSO) also show this response, which may therefore involve a ubiquitous mechanism. We also found that HMBA depresses the expression of endogenous globin genes in K562, the opposite of this differentiation inducer's effect on MELC.

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“…As mentioned above, once the MEL tumor cells reenter the erythroid differentiation program, they continue proliferating, but these cell cycles are limited to 5-6 divisions which are then followed by arrest in G1 (3). During the latter stages of this process we observed that the activities of CDK2 and CDK4 declined (Figure 2).…”

Section: Transition Ii: From Proliferating Differentiating Cells To Tmentioning

confidence: 74%

Reprogramming erythroleuekmia cells to terminal differentiation and terminal cell division

et al. 2000

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Commitment to erythroid differentiation by friend erythroleukemia cells: a stochastic analysis

Cited by 351 publications

References 9 publications

Deregulated expression of the PU.1 transcription factor blocks murine erythroleukemia cell terminal differentiation

Deregulated expression of the PU.1 transcription factor blocks murine erythroleukemia cell terminal differentiation

Induction by HMBA and DMSO of genes introduced into mouse erythroleukemia and other cell lines by transient transfection.

Reprogramming erythroleuekmia cells to terminal differentiation and terminal cell division

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