An insight into the post‐transcriptional control of gene expression in cell function

Osborne, Howard Beverley

doi:10.1016/s0248-4900(03)00029-7

Cited by 9 publications

(5 citation statements)

References 17 publications

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“…Finally, it is noteworthy that essentially parallel changes were observed at both the start and the end exons of the TNF-␣ and MCP-1 genes. Because Pol II recruitment along the gene is Along with increased transcription, mRNA stabilization may also raise mRNA levels (e.g., [12][13][14][15][16][17] ). Thus, we addressed whether this mechanism, rather than Pol II-driven gene transcription, might have caused the preferential LPS-mediated TNF-␣/MCP-1 mRNA increases in the setting of ARF.…”

Section: Discussionmentioning

confidence: 99%

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Endotoxin Mediates Recruitment of RNA Polymerase II to Target Genes in Acute Renal Failure

Naito

Bomsztyk

Zager

2008

Journal of the American Society of Nephrology

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Acute renal failure (ARF) sensitizes the kidney to endotoxin (LPS)-driven production of cytokines and chemokines. This study assessed whether this LPS hyperresponsiveness exists at the genomic level. Three heterogeneous mouse models of ARF were studied: Maleate nephrotoxicity, unilateral ureteral obstruction, and LPS preconditioning. In all cases, LPS was injected approximately 18 h after injury was induced, and over the next 0 to 90 min, RNA polymerase II recruitment to the genome at three LPS-responsive genes (TNF-␣, monocyte chemoattractant-1 [MCP-1], and heme oxygenase-1 [HO-1]) was assessed by chromatin immunoprecipitation. LPS hyperresponsiveness was noted in each model, measured by exaggerated increases in TNF-␣ and MCP-1 mRNA (approximately two to 10 times higher than LPS-injected controls). Corresponding increases in the recruitment of RNA polymerase II to the TNF-␣ and MCP-1 genes were observed, and increased trimethylation of histone 3 lysine 4 (H3K4m3) at these sites may have played a role in this recruitment. Conversely, recruitment of RNA polymerase II to the HO-1 gene was suppressed ("tolerance"), and no increase in H3K4m3 was observed at HO-1 exons. The ARF-induced changes in mRNA did not correlate with mRNA stability, suggesting the mechanistic importance of RNA polymerase II-mediated transcriptional events. In conclusion, LPS hyperresponsiveness after ARF is likely mediated at the genomic level, possibly by H3K4m3.

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Section: Discussionmentioning

confidence: 99%

“…However, it is not known whether enhanced transcription and/or stress-induced increases in mRNA stability [12][13][14][15][16][17] account for these increased transcript levels.…”

mentioning

confidence: 99%

Endotoxin Mediates Recruitment of RNA Polymerase II to Target Genes in Acute Renal Failure

Naito

Bomsztyk

Zager

2008

Journal of the American Society of Nephrology

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“…Similarly, removal of the poly(A) tail is often the first step in the degradation of the mRNA body; an mRNA with a long poly(A) tail is more stable than an mRNA with a short or no poly(A) tail. For a more detailed understanding of the mechanisms involved, please refer to the volume 95, Issue 3-4 of Biology of the Cell (Inge-Vechtomov et al, 2003;Kean, 2003;Linder, 2003;Osborne, 2003;Prevot et al, 2003;Schaeffer et al, 2003;Touriol et al, 2003). You could also refer to Bevilacqua et al, 2003. mRNA stability and translation are controlled through a complex network of RNA/protein interactions involving recognition of specific target mRNAs by RNA-BPs.…”

Section: Introductionmentioning

confidence: 99%

Post‐transcriptional regulation in cancer

Audic

Hartley

2004

Biology of the Cell

206

204

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Deregulation of gene expression is a hallmark of the cancer cell. Acquiring a new profile of expressed proteins may enable the cell to re-enter the cell cycle, or give them a growth or motility advantage over "normal cells". An efficient and rapid way to alter gene expression is via regulation of mRNAs already transcribed. Modifications of mRNA stability and/or translational efficiency are increasingly reported in cancer. mRNA stability and translation are controlled through a complex network of RNA/protein interactions involving recognition of specific target mRNAs by RNA-BPs. We review how alterations in regulatory sequences, RNA-BPs, or in upstream signalling pathways affect the stability and/or translational efficiency of mRNAs encoding proto-oncogenes, cytokines, cell cycle regulators and other regulatory proteins to promote tumorigenesis and cancer progression.A more thorough understanding of post-transcriptional mechanisms such as these will enable the design and development of specific therapies based on modulating the translation or stability of specific mRNAs.

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“…A plethora of different mechanisms modify the primary transcripts on their way to the protein (or non-coding RNA) that they eventually code for, see e.g. [22,55] for recent reviews. Most of these control mechanisms involve specific RNA-protein interactions that depend crucially on the recognition of sequence and/or structural features of the RNA [28].…”

Section: Introductionmentioning

confidence: 99%

The effect of RNA secondary structures on RNA-ligand binding and the modifier RNA mechanism: a quantitative model

Hackermüller¹,

Meisner²,

Auer³

et al. 2005

Gene

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RNA-ligand binding often depends crucially on the local RNA secondary structure at the binding site. We develop here a model that quantitatively predicts the effect of RNA secondary structure on effective RNA-ligand binding activities based on equilibrium thermodynamics and the explicit computations of partition functions for the RNA structures. A statistical test for the impact of a particular structural feature on the binding affinities follows directly from this approach. The formalism is extended to describing the effects of hybridizing small "modifier RNAs" to a target RNA molecule outside its ligand binding site. We illustrate the applicability of our approach by quantitatively describing the interaction of the mRNA stabilizing protein HuR with AU-rich elements [Meisner et al. (2004), Chem. Biochem. in press]. We discuss our model and recent experimental findings demonstrating the effectivity of modifier RNAs in vitro in the context of the current research activities in the field of non-coding RNAs. We speculate that modifier RNAs might also exist in nature; if so, they present an additional regulatory layer for fine-tuning gene expression that could evolve rapidly, leaving no obvious traces in the genomic DNA sequences.

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An insight into the post‐transcriptional control of gene expression in cell function

Cited by 9 publications

References 17 publications

Endotoxin Mediates Recruitment of RNA Polymerase II to Target Genes in Acute Renal Failure

Endotoxin Mediates Recruitment of RNA Polymerase II to Target Genes in Acute Renal Failure

Post‐transcriptional regulation in cancer

The effect of RNA secondary structures on RNA-ligand binding and the modifier RNA mechanism: a quantitative model

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