Poly(A)-binding proteins: Structure, domain organization, and activity regulation

Eliseeva, Irina A.; Lyabin, Dmitry N.; Ovchinnikov, Lev P.

doi:10.1134/s0006297913130014

Cited by 76 publications

(83 citation statements)

References 155 publications

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“…It was previously shown that PABP preferentially interacts with poly(A) or A-rich sequences (Eliseeva et al, 2013). The binding affinity increases as the A stretch gets longer (Eliseeva et al, 2013; Khanam et al, 2006; Kühn and Pieler, 1996; Sachs et al, 1987). Full-length PABP occupies an ∼25 nt A-tail as determined by nuclease digestion assay (Baer and Kornberg, 1983; Eliseeva et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

“…The binding affinity increases as the A stretch gets longer (Eliseeva et al, 2013; Khanam et al, 2006; Kühn and Pieler, 1996; Sachs et al, 1987). Full-length PABP occupies an ∼25 nt A-tail as determined by nuclease digestion assay (Baer and Kornberg, 1983; Eliseeva et al, 2013). In order to test an effect of PABP on uridylation, we carried out in vitro uridylation assays in the presence of recombinant PABPC1 (Figure 3).…”

Section: Resultsmentioning

confidence: 99%

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Uridylation by TUT4 and TUT7 Marks mRNA for Degradation

Lim

Chang

et al. 2014

Cell

259

320

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Summary Uridylation occurs pervasively on mRNAs, yet its mechanism and significance remain unknown. By applying TAIL-seq, we identify TUT4 and TUT7 (TUT4/7), also known as ZCCHC11 and ZCCHC6, respectively, as mRNA uridylation enzymes. Uridylation readily occurs on deadenylated mRNAs in cells. Consistently, purified TUT4/7 selectively recognize and uridylate RNAs with short A-tails (less than ∼25 nt) in vitro. PABPC1 antagonizes uridylation of polyadenylated mRNAs, contributing to the specificity for short A-tails. In cells depleted of TUT4/7, the vast majority of mRNAs lose the oligo-U-tails, and their half-lives are extended. Suppression of mRNA decay factors leads to the accumulation of oligo-uridylated mRNAs. In line with this, microRNA induces uridylation of its targets, and TUT4/7 are required for enhanced decay of microRNA targets. Our study explains the mechanism underlying selective uridylation of deadenylated mRNAs and demonstrates a fundamental role of oligo-U-tail as a molecular mark for global mRNA decay.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Uridylation by TUT4 and TUT7 Marks mRNA for Degradation

Lim

Chang

et al. 2014

Cell

259

320

View full text Add to dashboard Cite

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“…Within this segment of 8q22.2 is the gene PABPC1 , whose protein function is to bind the poly-A tail of messenger RNA (mRNA) in the nucleus and shuttle the transcript to the cytoplasm for translation (Eliseeva et al 2013). PABPC1-associated poly-A tails stimulate translation and stabilize mRNA in the cytoplasm and increased levels of PABPC1 may lead to excessive and oncogenic increases in the mRNA half-lives and thus increased potency of even a normal number of transcripts.…”

Section: Discussionmentioning

confidence: 99%

Canine urothelial carcinoma: genomically aberrant and comparatively relevant

et al. 2015

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Urothelial carcinoma (UC), also referred to as transitional cell carcinoma (TCC), is the most common bladder malignancy in both human and canine populations. In human UC, numerous studies have demonstrated the prevalence of chromosomal imbalances. Although the histopathology of the disease is similar in both species, studies evaluating the genomic profile of canine UC are lacking, limiting the discovery of key comparative molecular markers associated with driving UC pathogenesis. In the present study, we evaluated 31 primary canine UC biopsies by oligonucleotide array comparative genomic hybridization (oaCGH). Results highlighted the presence of three highly recurrent numerical aberrations: gain of dog chromosome (CFA) 13 and 36 and loss of CFA 19. Regional gains of CFA 13 and 36 were present in 97% and 84% of cases, respectively, and losses on CFA 19 were present in 77% of cases. Fluorescence in situ hybridization (FISH), using targeted bacterial artificial chromosome (BAC) clones and custom Agilent SureFISH probes, was performed to detect and quantify these regions in paraffin-embedded biopsy sections and urine-derived urothelial cells. The data indicate that these three aberrations are potentially diagnostic of UC. Comparison of our canine oaCGH data with that of 285 human cases identified a series of shared copy number aberrations. Using an informatics approach to interrogate the frequency of copy number aberrations across both species, we identified those that had the highest joint probability of association with UC. The most significant joint region contained the gene PABPC1, which should be considered further for its role in UC progression. In addition, cross-species filtering of genome-wide copy number data highlighted several genes as high-profile candidates for further analysis, including CDKN2A, S100A8/9, and LRP1B. We propose that these common aberrations are indicative of an evolutionarily conserved mechanism of pathogenesis and harbor genes key to urothelial neoplasia, warranting investigation for diagnostic, prognostic, and therapeutic applications.

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“…Newly synthesized mRNA is known to acquire a long poly(A) tail (up to ∼250 nucleotides [nt]) through canonical polyadenylation coupled to transcription, which facilitates mRNA export from the nucleus (Wahle and Keller 1996). In the cytoplasm, poly(A) tails are associated with cytoplasmic poly(A)-binding proteins (PABPCs) that stabilize mRNA by acting as a safeguard against multiple decay machineries and promote protein synthesis (Eliseeva et al 2013;Norbury 2013). Once mRNA is deadenylated to a certain threshold (∼25 nt), PABPC is released, and mRNA becomes translationally inactive and prone to degradation.…”

mentioning

confidence: 99%

mTAIL-seq reveals dynamic poly(A) tail regulation in oocyte-to-embryo development

et al. 2016

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Eukaryotic mRNAs are subject to multiple types of tailing that critically influence mRNA stability and translatability. To investigate RNA tails at the genomic scale, we previously developed TAIL-seq, but its low sensitivity precluded its application to biological materials of minute quantity. In this study, we report a new version of TAIL-seq (mRNA TAIL-seq [mTAIL-seq]) with enhanced sequencing depth for mRNAs (by ∼1000-fold compared with the previous version). The improved method allows us to investigate the regulation of poly(A) tails in Drosophila oocytes and embryos. We found that maternal mRNAs are polyadenylated mainly during late oogenesis, prior to fertilization, and that further modulation occurs upon egg activation. Wispy, a noncanonical poly(A) polymerase, adenylates the vast majority of maternal mRNAs, with a few intriguing exceptions such as ribosomal protein transcripts. By comparing mTAIL-seq data with ribosome profiling data, we found a strong coupling between poly(A) tail length and translational efficiency during egg activation. Our data suggest that regulation of poly(A) tails in oocytes shapes the translatomic landscape of embryos, thereby directing the onset of animal development. By virtue of the high sensitivity, low cost, technical robustness, and broad accessibility, mTAIL-seq will be a potent tool to improve our understanding of mRNA tailing in diverse biological systems.

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Poly(A)-binding proteins: Structure, domain organization, and activity regulation

Cited by 76 publications

References 155 publications

Uridylation by TUT4 and TUT7 Marks mRNA for Degradation

Uridylation by TUT4 and TUT7 Marks mRNA for Degradation

Canine urothelial carcinoma: genomically aberrant and comparatively relevant

mTAIL-seq reveals dynamic poly(A) tail regulation in oocyte-to-embryo development

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