Downregulation of histone H4 gene transcription during postnatal development in transgenic mice and at the onset of differentiation in transgenically derived calvarial osteoblast cultures

Gerbaulet, Stephan; Wijnen, André J. van; Aronin, Neil; Tassinari, Melissa S.; Lian, Jane B.; Stein, Janet L.

doi:10.1002/jcb.240490206

Cited by 11 publications

(8 citation statements)

References 48 publications

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“…Multiple histones (H2A, H2B, H4 and H1 histone-like protein) previously identified as downregulated during metacyclogenesis ( 65 , 66 ) were also identified as such in this analysis with H4 mRNA levels particularly depleted. The decrease in histone transcripts as the parasite enters the non-dividing stationary phase suggests a mode of regulation that is dependent on the cell cycle and is consistent with observations in higher eukaryotes that histone gene expression decreases in differentiated cells ( 67 , 68 ). Also consistent with previous findings, multiple β-tubulin family members were identified as downregulated ∼1.4-fold as the parasite becomes infective ( 69 ).…”

Section: Resultssupporting

confidence: 87%

Transcriptomic profiling of gene expression and RNA processing duringLeishmania majordifferentiation

Dillon¹,

Okrah²,

Hughitt³

et al. 2015

Nucleic Acids Res

100

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Protozoan parasites of the genus Leishmania are the etiological agents of leishmaniasis, a group of diseases with a worldwide incidence of 0.9–1.6 million cases per year. We used RNA-seq to conduct a high-resolution transcriptomic analysis of the global changes in gene expression and RNA processing events that occur as L. major transforms from non-infective procyclic promastigotes to infective metacyclic promastigotes. Careful statistical analysis across multiple biological replicates and the removal of batch effects provided a high quality framework for comprehensively analyzing differential gene expression and transcriptome remodeling in this pathogen as it acquires its infectivity. We also identified precise 5′ and 3′ UTR boundaries for a majority of Leishmania genes and detected widespread alternative trans-splicing and polyadenylation. An investigation of possible correlations between stage-specific preferential trans-splicing or polyadenylation sites and differentially expressed genes revealed a lack of systematic association, establishing that differences in expression levels cannot be attributed to stage-regulated alternative RNA processing. Our findings build on and improve existing expression datasets and provide a substantially more detailed view of L. major biology that will inform the field and potentially provide a stronger basis for drug discovery and vaccine development efforts.

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Section: Resultssupporting

confidence: 87%

Transcriptomic profiling of gene expression and RNA processing duringLeishmania majordifferentiation

Dillon¹,

Okrah²,

Hughitt³

et al. 2015

Nucleic Acids Res

100

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“…The latter Hist1 cluster was later replicating in 8/8 committed cell types in mouse and 5/6 in human (not lymphoblasts), and includes several core histone genes that were downregulated up to 2.5-fold in NPCs. These results are intriguing in light of previous reports of histone downregulation during development [28], as well as a hyperdynamic chromatin phenotype in ESCs that involves higher exchange rates of histone H1 [29] and is required for efficient somatic cell nuclear reprogramming in Xenopus oocytes [30]. Importantly, all of the histone H1 genes are found in this cluster, suggesting that regulation of global H1 abundance may provide a mechanism for the overall chromatin compaction and consolidation of replication timing observed during neural differentiation [3]–[5].…”

Section: Resultssupporting

confidence: 62%

Replication Timing: A Fingerprint for Cell Identity and Pluripotency

et al. 2011

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Many types of epigenetic profiling have been used to classify stem cells, stages of cellular differentiation, and cancer subtypes. Existing methods focus on local chromatin features such as DNA methylation and histone modifications that require extensive analysis for genome-wide coverage. Replication timing has emerged as a highly stable cell type-specific epigenetic feature that is regulated at the megabase-level and is easily and comprehensively analyzed genome-wide. Here, we describe a cell classification method using 67 individual replication profiles from 34 mouse and human cell lines and stem cell-derived tissues, including new data for mesendoderm, definitive endoderm, mesoderm and smooth muscle. Using a Monte-Carlo approach for selecting features of replication profiles conserved in each cell type, we identify “replication timing fingerprints” unique to each cell type and apply a k nearest neighbor approach to predict known and unknown cell types. Our method correctly classifies 67/67 independent replication-timing profiles, including those derived from closely related intermediate stages. We also apply this method to derive fingerprints for pluripotency in human and mouse cells. Interestingly, the mouse pluripotency fingerprint overlaps almost completely with previously identified genomic segments that switch from early to late replication as pluripotency is lost. Thereafter, replication timing and transcription within these regions become difficult to reprogram back to pluripotency, suggesting these regions highlight an epigenetic barrier to reprogramming. In addition, the major histone cluster Hist1 consistently becomes later replicating in committed cell types, and several histone H1 genes in this cluster are downregulated during differentiation, suggesting a possible instrument for the chromatin compaction observed during differentiation. Finally, we demonstrate that unknown samples can be classified independently using site-specific PCR against fingerprint regions. In sum, replication fingerprints provide a comprehensive means for cell characterization and are a promising tool for identifying regions with cell type-specific organization.

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“…The LacZ expression pattern driven by the Hinfp promoter (Fig. 4) is comparable to results obtained with distinct transgenes under control of a representative human histone H4 promoter (Gerbaulet et al, 1992; van Wijnen et al, 1991). The latter studies revealed proliferation-related transgene expression reflecting histone H4 promoter activity in different mouse tissues and cell types, including cells from cranial tissues (e.g., calvaria, brain).…”

Section: Resultssupporting

confidence: 73%

“…This down regulation occurs presumably by destabilization of histone mRNA when DNA synthesis ceases upon completion of the first S phase (Osley, 1991; Stein et al, 1984). In vivo studies on histone H4 gene transcription have been limited to work with transgenic mice that focused on mid-gestation and later stages of fetal development in both osseous and non-osseous (e.g., liver, spleen) tissues (Gerbaulet et al, 1992; van Wijnen et al, 1991). In addition, a few studies have examined mouse histone H4 gene transcription in cultured cells (Seiler-Tuyns and Paterson, 1987; van der Meijden et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Functional coupling of transcription factor HiNF-P and histone H4 gene expression during pre- and post-natal mouse development

Liu

Xie

Hussain

et al. 2011

Gene

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Transcription factor Histone Nuclear Factor P (HiNF-P; gene symbol Hinfp) mediates cell cycle control of histone H4 gene expression to support the packaging of newly replicated DNA as chromatin. The HiNF-P/p220NPAT complex controls multiple H4 genes in established human cell lines and is critical for cell proliferation. The mouse HinfpLacZ null allele causes early embryonic lethality due to a blastocyst defect. However, neither Hinfp function nor its temporal expression relative to histone H4 genes during fetal development has been explored. Here, we establish that expression of Hinfp is biologically coupled with expression of twelve functional mouse H4 genes during pre- and post-natal tissue-development. Both Hinfp and H4 genes are robustly expressed at multiple embryonic (E) days (from E5.5 to E15.5), coincident with ubiquitous LacZ staining driven by the Hinfp promoter. Five highly expressed mouse H4 genes (Hist1h4d, Histh4f, Hist1h4m and Hist2h4) account for >90% of total histone H4 mRNA throughout development. Post-natal expression of H4 genes in mice is most evident in lung, spleen, thymus and intestine, and with few exceptions (e.g., adult liver) correlates with Hinfp gene expression. Histone H4 gene expression decreases but Hinfp levels remain constitutive upon cell growth inhibition in culture. The in vivo co-expression of Hinfp and histone H4 genes is consistent with the biological function of Hinfp as a principal transcriptional regulator of histone H4 gene expression during mouse development.

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Downregulation of histone H4 gene transcription during postnatal development in transgenic mice and at the onset of differentiation in transgenically derived calvarial osteoblast cultures

Cited by 11 publications

References 48 publications

Transcriptomic profiling of gene expression and RNA processing duringLeishmania majordifferentiation

Transcriptomic profiling of gene expression and RNA processing duringLeishmania majordifferentiation

Replication Timing: A Fingerprint for Cell Identity and Pluripotency

Functional coupling of transcription factor HiNF-P and histone H4 gene expression during pre- and post-natal mouse development

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