Cytoplasmic polyadenylation by TENT5A is required for proper bone formation

Gewartowska, Olga; Aranaz-Novaliches, Goretti; Krawczyk, Paweł S.; Mroczek, Seweryn; Kusio-Kobiałka, Monika; Tarkowski, Bartosz; Špoutil, František; Benada, Oldřich; Kofroňová, Olga; Szwedziak, Piotr; Cysewski, Dominik; Gruchota, Jakub; Szpila, Marcin; Chlebowski, Aleksander; Sedláček, Radislav; Procházka, Jan; Dziembowski, Andrzej

doi:10.1016/j.celrep.2021.109015

Cited by 33 publications

(58 citation statements)

References 49 publications

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“…2, E and F). TENT5A, a poly(A) polymerase in which multiple coding variants have been linked to autosomal-recessive osteogenesis imperfecta (32), polyadenylates and increases expression in osteoblasts of the collagen genes COL1A1 and COL1A2 and other genes mutated in this disease (33). MUC1 VNTR cause autosomal-dominant tubulointerstitial kidney disease (35).…”

Section: Genementioning

confidence: 99%

Protein-coding repeat polymorphisms strongly shape diverse human phenotypes

Mukamel

Handsaker

Sherman

et al. 2021

Science

127

163

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Repeats associated with phenotype The degree to which repeated sequences within a genome affect human phenotypes has been difficult to establish. Mukamel et al . examined thousands of genomes in the UK Biobank and found that some of the largest effects of common genetic variants on human phenotypes, including those with clinical relevance, arise from protein-coding repeat polymorphisms (see the Perspective by Gymrek and Goren). Mapping the effects of the size and copy number of these repeated protein domains links genetic variation to human phenotypes, including lipoprotein(a) concentration, height, and male pattern balding. Furthermore, the alleles and frequencies of these repeated sequences differ between individuals of African and European descent, resulting in differences between the populations with clinical relevance for traits including lipoprotein(a) levels, a risk factor for coronary artery disease. —LMZ

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Section: Genementioning

confidence: 99%

Protein-coding repeat polymorphisms strongly shape diverse human phenotypes

Mukamel

Handsaker

Sherman

et al. 2021

Science

127

163

View full text Add to dashboard Cite

show abstract

“…Changes in poly(A) tail length chiefly contribute to the stability and translation of mRNA ( Passmore & Coller, 2021 ). Poly(A) tail elongation has been shown to promote translation in biological contexts as diverse as oocyte maturation, early embryonic development, neuronal plasticity, bone formation, cell proliferation, senescence, inflammation, metabolism, circadian gene expression, hibernation, and cancer (reviewed in Kojima et al [2012] , D’Ambrogio et al [2014] , Ivshina et al [2014] , Grabek et al [2015] , Kozlov et al [2021] , Gewartowska et al [2021] ). This process is typically controlled by the cytoplasmic polyadenylation element–binding (CPEB) family of proteins, which bind to U-rich cytoplasmic polyadenylation elements (CPEs) in the 3′ UTR of transcripts ( Ivshina et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Ataxin-2, Twenty-four, and Dicer-2 are components of a noncanonical cytoplasmic polyadenylation complex

et al. 2022

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Cytoplasmic polyadenylation is a mechanism to promote mRNA translation in a wide variety of biological contexts. A canonical complex centered around the conserved RNA-binding protein family CPEB has been shown to be responsible for this process. We have previously reported evidence for an alternative noncanonical, CPEB-independent complex in Drosophila, of which the RNA-interference factor Dicer-2 is a component. Here, we investigate Dicer-2 mRNA targets and protein cofactors in cytoplasmic polyadenylation. Using RIP-Seq analysis, we identify hundreds of potential Dicer-2 target transcripts, ∼60% of which were previously found as targets of the cytoplasmic poly(A) polymerase Wispy, suggesting widespread roles of Dicer-2 in cytoplasmic polyadenylation. Large-scale immunoprecipitation revealed Ataxin-2 and Twenty-four among the high-confidence interactors of Dicer-2. Complex analyses indicated that both factors form an RNA-independent complex with Dicer-2 and mediate interactions of Dicer-2 with Wispy. Functional poly(A)-test analyses showed that Twenty-four and Ataxin-2 are required for cytoplasmic polyadenylation of a subset of Dicer-2 targets. Our results reveal components of a novel cytoplasmic polyadenylation complex that operates during Drosophila early embryogenesis.

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“…Thus, the starfish homologue of TENT4 may generate the 5’ modifications in the non-canonical poly(A) tails. In addition, TENT5 families mediate the cytoplasmic polyadenylation of collagen mRNAs required for bone mineralisation (49) and immunoglobulin mRNAs (50) in mammals. These families may also participate in the non-canonical polyadenylation, exhibiting a high percentage of A residues, especially at the 3’ region in the starfish cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Recycling of uridylated mRNAs in starfish embryos

Yamazaki

Furuichi

Katagiri

et al. 2022

Preprint

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In eukaryotes, mRNAs with long poly(A) tails are translationally active, whereas deadenylation of the tails decreases translation and uridylation of the short poly(A) tails causes the mRNA to be degraded. In this study, we confirmed that maternal cyclin B mRNAs with long poly(A) tails in blastula embryos of invertebrate starfish were deadenylated and uridylated, followed by decay. In starfish oocytes, however, cyclin B mRNAs with uridylated short poly(A) tails are stable. They are polyadenylated and translationally active immediately following hormonal stimulation for resumption of meiosis. Similarly, maternal ribosomal protein mRNAs, Rps29 and Rpl27a, which become uridylated following deadenylation upon hormonal stimulation, remain stable even after fertilisation and early development. At the morula stage, the uridylated maternal ribosomal protein mRNAs are modified to yield non-canonical poly (A) tails rich in U and G residues in the 5' region and in A residues at the 3' end, rendering them translationally active. These results indicate that the fates of uridylated mRNAs in starfish are decay and/or recycling.

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Cytoplasmic polyadenylation by TENT5A is required for proper bone formation

Cited by 33 publications

References 49 publications

Protein-coding repeat polymorphisms strongly shape diverse human phenotypes

Protein-coding repeat polymorphisms strongly shape diverse human phenotypes

Ataxin-2, Twenty-four, and Dicer-2 are components of a noncanonical cytoplasmic polyadenylation complex

Recycling of uridylated mRNAs in starfish embryos

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