Maintenance of Open Chromatin and Selective Genomic Occupancy at the Cell Cycle-Regulated Histone H4 Promoter during Differentiation of HL-60 Promyelocytic Leukemia Cells

Hovhannisyan, Hayk; Cho, Brian; Mitra, Partha; Montecino, Martín; Stein, Gary S.; Wijnen, André J. van; Stein, Janet L.

doi:10.1128/mcb.23.4.1460-1469.2003

Cited by 25 publications

(22 citation statements)

References 37 publications

(40 reference statements)

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“…Our immunofluorescence data reveal that a significant fraction of HiNF-P is also located at a large number of other smaller subnuclear foci (2). We have shown that expression of HiNF-P is proliferation related (1,8,9). Depletion of HiNF-P decreases histone H4 mRNA levels in asynchronous cells and delays progression into S phase following serum stimulation of quiescent cells (1).…”

Section: Introductionmentioning

confidence: 60%

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

et al. 2007

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HiNF-P and its cofactor p220NPAT are principal factors regulating histone gene expression at the G 1 -S phase cell cycle transition. Here, we have investigated whether HiNF-P controls other cell cycle-and cancer-related genes. We used cDNA microarrays to monitor responsiveness of gene expression to small interfering RNA-mediated depletion of HiNF-P. Candidate HiNF-P target genes were examined for the presence of HiNF-P recognition motifs, in vitro HiNF-P binding to DNA, and in vivo association by chromatin immunoprecipitations and functional reporter gene assays. Of 177 proliferation-related genes we tested, 20 are modulated in HiNF-P-depleted cells and contain putative HiNF-P binding motifs. We validated that at least three genes (i.e., ATM, PRKDC, and CKS2) are HiNF-P dependent and provide data indicating that the DNA damage response is altered in HiNF-P-depleted cells. We conclude that, in addition to histone genes, HiNF-P also regulates expression of nonhistone targets that influence competency for cell cycle progression. [Cancer Res 2007;67(21):10334-42]

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Section: Introductionmentioning

confidence: 60%

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

et al. 2007

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“…HINFP is a ubiquitous regulator of histone H4 gene expression in all proliferating cell types examined to date, and the protein is down-regulated in post-proliferative differentiated cells (11,13,15,36). HINFP transduces cyclin E/CDK2 signals into transcriptional responses through interactions with its obligatory coactivator p220…”

Section: Discussionmentioning

confidence: 99%

The histone gene activator HINFP is a nonredundant cyclin E/CDK2 effector during early embryonic cell cycles

Xie

Medina

Zhang

et al. 2009

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

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Competency for DNA replication is functionally coupled to the activation of histone gene expression at the onset of S phase to form chromatin. Human histone nuclear factor P (HiNF-P; gene symbol HINFP) bound to its cyclin E/cyclin-dependent kinase 2 (CDK2) responsive coactivator p220 NPAT is a key regulator of multiple human histone H4 genes that encode a major subunit of the nucleosome. Induction of the histone H4 transcription factor (HINFP)/p220 NPAT coactivation complex occurs in parallel with the CDK-dependent release of pRB from E2F at the restriction point. Here, we show that the downstream CDK-dependent cell cycle effector HINFP is genetically required and, in contrast to the CDK2/cyclin E complex, cannot be compensated. We constructed a mouse Hinfp-null mutation and found that heterozygous Hinfp mice survive, indicating that 1 allele suffices for embryogenesis. Homozygous loss-of-function causes embryonic lethality: No homozygous Hinfp-null mice are obtained at or beyond embryonic day (E) 6.5. In blastocyst cultures, Hinfp-null embryos exhibit a delay in hatching, abnormal growth, and loss of histone H4 gene expression. Our data indicate that the CDK2/cyclin E/p220 NPAT / HINFP/histone gene signaling pathway at the G1/S phase transition is an essential, nonredundant cell cycle regulatory mechanism that is established early in embryogenesis.blastocyst ͉ development ͉ embryogenesis ͉ p220 NPAT ͉ human embryonic stem cells

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“…Gene expression patterns were identified by using hierarchical cluster analysis of row-wise standardized data with dCHIP software (42). Affymetrix microarrays (Hu-U133Plus2 chips) and ChIP assays were performed as described (43)(44)(45).…”

Section: Methodsmentioning

confidence: 99%

Mitotic retention of gene expression patterns by the cell fate-determining transcription factor Runx2

Young

Hassan

Yang

et al. 2007

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

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During cell division, cessation of transcription is coupled with mitotic chromosome condensation. A fundamental biological question is how gene expression patterns are retained during mitosis to ensure the phenotype of progeny cells. We suggest that cell fate-determining transcription factors provide an epigenetic mechanism for the retention of gene expression patterns during cell division. Runx proteins are lineage-specific transcription factors that are essential for hematopoietic, neuronal, gastrointestinal, and osteogenic cell fates. Here we show that Runx2 protein is stable during cell division and remains associated with chromosomes during mitosis through sequence-specific DNA binding. Using siRNA-mediated silencing, mitotic cell synchronization, and expression profiling, we identify Runx2-regulated genes that are modulated postmitotically. Novel target genes involved in cell growth and differentiation were validated by chromatin immunoprecipitation. Importantly, we find that during mitosis, when transcription is shut down, Runx2 selectively occupies target gene promoters, and Runx2 deficiency alters mitotic histone modifications. We conclude that Runx proteins have an active role in retaining phenotype during cell division to support lineage-specific control of gene expression in progeny cells.L ineage commitment and cell proliferation are critical for normal tissue development. Preservation of phenotype during clonal expansion of committed cells necessitates the faithful segregation of chromosomes and the conveyance of lineage-specific gene regulatory machinery to progeny cells. Mitosis involves nuclear reorganization, global chromosome condensation, and transcription silencing and occurs concomitant with protein degradation and/or displacement of many regulatory factors from chromosomes (1-4). One fundamental question is how cells are programmed to sustain phenotypic gene expression patterns after cell division when transcriptional competency is restored in progeny cells.Cell fate is determined in response to extracellular cues by lineage-specific master regulators that include the Runx family of transcription factors. In mammals, these proteins are required for development of hematopoietic (Runx1), osteogenic (Runx2), and gastrointestinal and neuronal (Runx3) cell lineages (5-11). Runx factors integrate cell signaling pathways (e.g., TGF-␤/bone morphogenetic protein and Yes/Src) and recruit chromatin-modifying enzymes (e.g., histone deacetylases, histone acetyltransferases, SWI/SNF, SuVar139) to modulate promoter accessibility within a nucleosomal context (10,(12)(13)(14)(15)(16)(17). Runx proteins function as promoter-bound scaffolds that organize the regulatory machinery for gene expression within punctate subnuclear domains during interphase (18,19). Pathological perturbations in the organization of these domains are linked with altered development and tumorigenesis (10,(20)(21)(22)(23)(24)(25)(26)(27)(28)(29). Temporal and spatial changes of these architecturally organized Runx domains occur during...

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Maintenance of Open Chromatin and Selective Genomic Occupancy at the Cell Cycle-Regulated Histone H4 Promoter during Differentiation of HL-60 Promyelocytic Leukemia Cells

Cited by 25 publications

References 37 publications

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

The histone gene activator HINFP is a nonredundant cyclin E/CDK2 effector during early embryonic cell cycles

Mitotic retention of gene expression patterns by the cell fate-determining transcription factor Runx2

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