Developmental stage–specific epigenetic control of human β-globin gene expression is potentiated in hematopoietic progenitor cells prior to their transcriptional activation

Bottardi, Stefania; Aumont, Angélique; Grosveld, Frank; Milot, Éric

doi:10.1182/blood-2003-05-1540

Cited by 61 publications

(91 citation statements)

References 63 publications

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“…Specific epigenetic marking by histone modification is already known to occur in multipotent stem cells and to be a consequence of the binding of transcription factors that are involved in lineage choice. (18)(19)(20)(21) According to our model, transcription factors that are expressed in ES cells (gene C in Fig. 4) would have a similar role in establishing epigenetic marks.…”

Section: Hypotheses Localised Epigenetic Marking As a Determinant Of mentioning

confidence: 85%

The epigenetic basis for embryonic stem cell pluripotency

Szutorisz

Dillon

2005

BioEssays

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SummaryAs well as having the remarkable ability to differentiate into all of the cell types in the embryo, embryonic stem (ES) cells also have the capacity to divide and self-renew. Maintenance of pluripotency through repeated cell divisions indicates that the developmental plasticity of ES cells has a specific epigenetic basis. We propose that tightly localised regions of histone modification are formed in ES cells by binding of sequence-specific transcription factors at genes that are destined for expression at later stages of differentiation. These 'early transcription competence marks' would help to maintain pluripotency by preventing the spread of repressive chromatin modifications. We further propose that the presence of discrete histone modification marks in pluripotent cells facilitates the binding of lineage-specific and general transcription factors to the marked regions as ES cells commit to different fates. By helping to organise the precisely timed responses of genes to the signals that determine lineage choice, the gene-specific localised epigenetic marks would play a key role in the establishment of complex gene expression programmes in differentiating cells.

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Section: Hypotheses Localised Epigenetic Marking As a Determinant Of mentioning

confidence: 85%

The epigenetic basis for embryonic stem cell pluripotency

Szutorisz

Dillon

2005

BioEssays

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“…Furthermore, we observed that chromatin activation is established and maintained by gene-and developmental-specific patterns of histone covalent modifications. 19 These observations suggest that hub-like globin genes are independently potentiated in HPCs, presumably through histone modifying activities recruited at specific regulatory regions by lineage-specific TFs. At the time we felt that GATA-1 and NF-E2 were good candidates because they: (1) are erythroid-specific TFs that interact with CBP at the b-globin locus; 37,38 and (2) are expressed at low level in HPCs.…”

Section: B-globin Gene Potentiation: the Role Of Lineage-specific Tfsmentioning

confidence: 94%

Section: Potentiation and Gene Priming In Hpcsmentioning

confidence: 99%

“…It is in fact proposed that most of the hematopoietic-specific genes are potentiated before their transcriptional activation in mature cells, [19][20][21] a mechanism that would protect these genes from epigenetic silencing. 19,22 Gene potentiation has been linked to histone covalent modifications of the locus of interest. For example, a discrete site of the B-cell specific mouse l5-VpreB1 locus 23,24 is marked by histone H3 acetylation and lysine 4 methylation (both marks of active chromatin) in ES cells.…”

Section: Potentiation and Gene Priming In Hpcsmentioning

confidence: 99%

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Lineage-Specific Transcription Factors in Multipotent Hematopoietic Progenitors: A Little Bit Goes a Long Way

Bottardi¹,

Ghiam²,

Bergeron³

et al. 2007

Cell Cycle

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“…Amplification of the HS4 gene by PCR was performed used sense primer (5Ј-TGG CAT CTA GCG CAA TGA CTT-3Ј) and antisense primer (5Ј-GGG CAA GCC ATC TCA TAG CTG-3Ј), which have been used in previous analyses of this region (24).…”

Section: Amplification Of Hcmv Dna By Ie-pcrmentioning

confidence: 99%

Latency, chromatin remodeling, and reactivation of human cytomegalovirus in the dendritic cells of healthy carriers

Reeves

MacAry

Lehner

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

321

412

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Human cytomegalovirus (HCMV) persists as a subclinical, lifelong infection in the normal human host, but reactivation from latency in immunocompromised subjects results in serious disease. Latency and reactivation are defining characteristics of the herpesviruses and are key to understanding their biology; however, the precise cellular sites in which HCMV is carried and the mechanisms regulating its latency and reactivation during natural infection remain poorly understood. Here we present evidence, based entirely on direct analysis of material isolated from healthy virus carriers, to show that myeloid dendritic cell (DC) progenitors are sites of HCMV latency and that their ex vivo differentiation to a mature DC phenotype is linked with reactivation of infectious virus resulting from differentiation-dependent chromatin remodeling of the viral major immediate-early promoter. Thus, myeloid DC progenitors are a site of HCMV latency during natural persistence, and there is a critical linkage between their differentiation to DC and transcriptional reactivation of latent virus, which is likely to play an important role in the pathogenesis of HCMV infection. P rimary infection of healthy individuals with human cytomegalovirus (HCMV) is often asymptomatic and results in lifelong persistence in the host, a characteristic of all herpes viruses. However, primary infection and reactivation of latent HCMV causes serious disease in immunosuppressed transplant recipients and in advanced HIV infection (1-3). Transfusionmediated HCMV disease can be prevented by leukocyte depletion (4) of blood, but infectious virus cannot be detected in the blood of healthy carriers, suggesting that HCMV is transmitted as latent virus in the peripheral blood leukocyte population. Accumulating evidence has shown that HCMV is carried latently in mononuclear cells of the myeloid lineage during lifelong latency in naturally infected individuals (5-8). Differentiation of monocytes to macrophages in vitro is reported to induce immediate-early (IE) lytic gene expression from latent virus (9), and groups have intermittently reported that infectious virus can be recovered after differentiation of monocytes to macrophages through explant culture (10) and, more recently, by allogeneic T cell stimulation (11), suggesting that reactivation of latent virus is associated with both the differentiation and activation state of myeloid cells.The major IE genes of HCMV, driven by the viral major IE promoter͞enhancer (MIEP), are the two most abundantly transcribed genes at IE times of virus lytic infection (12), and their proteins play a critical role in control of viral early and late gene expression (for review, see ref. 12). Consistent with the differentiation-dependent induction of IE gene expression observed above, there is a clear correlation between the differentiation state of the cell and the regulation of HCMV IE gene expression in vitro. Thus, in transfection assays, the MIEP is transcriptionally repressed in undifferentiated but transcriptionally active ...

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Developmental stage–specific epigenetic control of human β-globin gene expression is potentiated in hematopoietic progenitor cells prior to their transcriptional activation

Cited by 61 publications

References 63 publications

The epigenetic basis for embryonic stem cell pluripotency

The epigenetic basis for embryonic stem cell pluripotency

Lineage-Specific Transcription Factors in Multipotent Hematopoietic Progenitors: A Little Bit Goes a Long Way

Latency, chromatin remodeling, and reactivation of human cytomegalovirus in the dendritic cells of healthy carriers

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