RNA Destabilization by the Granulocyte Colony-Stimulating Factor Stem-Loop Destabilizing Element Involves a Single Stem-Loop That Promotes Deadenylation

Putland, Rodney A.; Sassinis, T. A.; Harvey, John S.; Diamond, Peter; Coles, Leeanne S.; Brown, Cheryl Y.; Goodall, Gregory J.

doi:10.1128/mcb.22.6.1664-1673.2002

Cited by 35 publications

(23 citation statements)

References 30 publications

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“…While prototype AREs, as in GM-CSF mRNA, reside in a narrow region (50), the more complex situation of IL-6 mRNA is not unique. Studies of G-CSF mRNA identified a destabilizing element adjacent to AREs that forms a stem-loop and prevents mRNA stabilization by the calcium ionophore A23187 (3,46). The sequence and folding of the putative IL-6 mRNA stem-loop are clearly distinct from those in G-CSF mRNA.…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that many individual mRNAs comprise either unpredicted ARE variants or other unknown destabilizing sequences. Even classical AREs are usually imbedded in neighboring sequence elements that are conserved in evolution but differ for each gene (11), and in several cases, such as G-CSF (46), TNF-␣ (53), and endothelin-1 (40), adjacent regions contribute to rapid mRNA degradation.…”

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confidence: 99%

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Destabilization of Interleukin-6 mRNA Requires a Putative RNA Stem-Loop Structure, an AU-Rich Element, and the RNA-Binding Protein AUF1

Paschoud¹,

Dogar²,

Kuntz³

et al. 2006

Molecular and Cellular Biology

137

135

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Interleukin-6 mRNA is unstable and degraded with a half-life of 30 min. Instability determinants can entirely be attributed to the 3 untranslated region. By grafting segments of this region to stable green fluorescent protein mRNA and subsequent scanning mutagenesis, we have identified two conserved elements, which together account for most of the instability. The first corresponds to a short noncanonical AU-rich element. The other, 80 nucleotides further 5, comprises a sequence predicted to form a stem-loop structure. Neither element alone was sufficient to confer full instability, suggesting that they might cooperate. Overexpression of myc-tagged AUF1 p37 and p42 isoforms as well as suppression of endogenous AUF1 by RNA interference stabilized interleukin-6 mRNA. Both effects required the AU-rich instability element. Similarly, the proteasome inhibitor MG132 stabilized interleukin-6 mRNA probably through an increase of AUF1 levels. The mRNA coimmunoprecipitated specifically with myc-tagged AUF1 p37 and p42 in cell extracts but only when the AU-rich instability element was present. These results indicate that AUF1 binds to the AU-rich element in vivo and promotes IL-6 mRNA degradation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Destabilization of Interleukin-6 mRNA Requires a Putative RNA Stem-Loop Structure, an AU-Rich Element, and the RNA-Binding Protein AUF1

Paschoud¹,

Dogar²,

Kuntz³

et al. 2006

Molecular and Cellular Biology

137

135

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“…The sequence with 4C, but not that with 3C, could interfere with this stem-loop formation by forming another, although less stable, stem-loop structure involving some of the same nucleotides. Stem-loop structures in the 3'UTR have been shown to be important determinants of message stability in some genes (Putland et al 2002). C-rich sequences are in some cases important for post-transcriptional regulation as exemplified by the α2-globin and collagen α1 genes (Weiss and Liebhaber 1995;Stefanovic et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Common variations in noncoding regions of the human natriuretic peptide receptor A gene have quantitative effects

et al. 2003

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Genetic susceptibility to common conditions, such as essential hypertension and cardiac hypertrophy, is probably determined by various combinations of small quantitative changes in the expression of many genes. NPR1, coding for natriuretic peptide receptor A (NPRA), is a potential candidate, because NPRA mediates natriuretic, diuretic, and vasorelaxing actions of the nariuretic peptides, and because genetically determined quantitative changes in the expression of this gene affect blood pressure and heart weight in a dose-dependent manner in mice. To determine whether there are common quantitative variants in human NPR1, we have sequenced the entire human NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript NPR1 gene and identified 10 polymorphic sites in its non-coding sequence by using DNA from 34 unrelated human individuals. Five of the sites are single nucleotide polymorphisms; the remaining five are length polymorphisms, including a highly variable complex dinucleotide repeat in intron 19. There are three common haplotypes 5' to this dinucleotide repeat and three 3' to it, but the 5' haplotypes and 3' haplotypes appear to be randomly associated. Transient expression analysis in cultured cells of reporter plasmids with the proximal promoter sequences of NPR1 and its 3' untranslated regions showed that these polymorphisms have functional effects. We conclude that common NPR1 alleles can alter expression of the gene as much as two-fold and could therefore significantly affect genetic risks for essential hypertension and cardiac hypertrophy in humans.

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“…7D) at positions 1371-1386. A single stem loop in the 3ЈUTR of granulocyte colony-stimulating factor mRNA has been reported recently to promote deadenylation and destabilization (Putland et al, 2002). Except for this potential stem-loop structure, no known deadenylation or instability elements are contained in this sequence.…”

Section: Discussionmentioning

confidence: 99%

Zygotic control of maternal cyclin A1 translation and mRNA stability

Audic

Garbrecht

Fritz

et al. 2002

Developmental Dynamics

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Cyclin mRNAs are unstable in the adult cell cycle yet are stable during the first 12 cell divisions in Xenopus laevis. We recently reported that cyclin A1 and B2 maternal mRNAs are deadenylated upon completion of the 12th division (Audic et al. [2001] Mol. Cell Biol. 21: 1662-1671). Deadenylation is mediated by the 3 untranslated region (UTR) of the mRNA and precedes the terminal disappearance of the cyclin proteins, with both processes requiring zygotic transcription. The purpose of the current study was (1) to ask whether deadenylation leads to translational repression and/or destabilization of endogenous cyclin A1 and B2 mRNAs, and (2) to further characterize the regulatory sequences required. We show that zygote-driven deadenylation leads to translational repression and mRNA destabilization. A 99-nucleotide region of the 3UTR of the cyclin A1 mRNA mediates both deadenylation and destabilization. Surprisingly, two AU-rich consensus elements within this region are dispensable for this activity. These results suggest that zygote-dependent deadenylation, translational repression, and mRNA destabilization by means of novel 3UTR elements contribute to the disappearance of maternal cyclins. They also suggest that translational control of cyclins may play a role in the transition to the adult cell cycle. These data concur with previous studies in Drosophila showing that zygote-mediated degradation of maternal cdc25 mRNA may be a general mechanism whereby transition to the adult cell cycle proceeds.

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RNA Destabilization by the Granulocyte Colony-Stimulating Factor Stem-Loop Destabilizing Element Involves a Single Stem-Loop That Promotes Deadenylation

Cited by 35 publications

References 30 publications

Destabilization of Interleukin-6 mRNA Requires a Putative RNA Stem-Loop Structure, an AU-Rich Element, and the RNA-Binding Protein AUF1

Destabilization of Interleukin-6 mRNA Requires a Putative RNA Stem-Loop Structure, an AU-Rich Element, and the RNA-Binding Protein AUF1

Common variations in noncoding regions of the human natriuretic peptide receptor A gene have quantitative effects

Zygotic control of maternal cyclin A1 translation and mRNA stability

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