JZUS - Journal of Zhejiang University SCIENCE

Journal of Zhejiang University SCIENCE B 2014 Vol.15 No.5 P.429-437

The polyadenylation code: a unified model for the regulation of mRNA alternative polyadenylation*

Author(s): Ryan Davis, Yongsheng Shi
Affiliation(s): . Department of Microbiology and Molecular Genetics, School of Medicine, University of California, Irvine, Irvine, CA 92697, USA
Corresponding email(s): yongshes@uci.edu
Key Words: mRNA, Alternative polyadenylation (APA), Polyadenylation site (PAS)

Share this article to： More <<< Previous Article \|Next Article >>>

Ryan Davis, Yongsheng Shi. The polyadenylation code: a unified model for the regulation of mRNA alternative polyadenylation[J]. Journal of Zhejiang University Science B, 2014, 15(5): 429-437.

@article{title="The polyadenylation code: a unified model for the regulation of mRNA alternative polyadenylation",
author="Ryan Davis, Yongsheng Shi",
journal="Journal of Zhejiang University Science B",
volume="15",
number="5",
pages="429-437",
year="2014",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1400076"
}

%0 Journal Article
%T The polyadenylation code: a unified model for the regulation of mRNA alternative polyadenylation
%A Ryan Davis
%A Yongsheng Shi
%J Journal of Zhejiang University SCIENCE B
%V 15
%N 5
%P 429-437
%@ 1673-1581
%D 2014
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1400076

TY - JOUR
T1 - The polyadenylation code: a unified model for the regulation of mRNA alternative polyadenylation
A1 - Ryan Davis
A1 - Yongsheng Shi
J0 - Journal of Zhejiang University Science B
VL - 15
IS - 5
SP - 429
EP - 437
%@ 1673-1581
Y1 - 2014
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1400076

Abstract
Chinese Summary
Academic Network
Reviewer Comment

Abstract: The majority of eukaryotic genes produce multiple mRNA isoforms with distinct 3′ ends through a process called mRNA alternative polyadenylation (APA). Recent studies have demonstrated that APA is dynamically regulated during development and in response to environmental stimuli. A number of mechanisms have been described for APA regulation. In this review, we attempt to integrate all the known mechanisms into a unified model. This model not only explains most of previous results, but also provides testable predictions that will improve our understanding of the mechanistic details of APA regulation. Finally, we briefly discuss the known and putative functions of APA regulation.

多腺苷酸化之密码：调解mRNA可变聚腺苷酸化的统一模型

本文概要：真核生物的大部分基因都通过可变聚腺苷酸化（APA）而产生多种不同的mRNA 3'端。近期的研究表明，可变聚腺苷酸化在组织发展中被动态调节，并且会受环境刺激而自动调节。现有文献中表述了多种调节机制。本文整合所有现有的调节机制模型，进而提出一个综合的统一模型。这个模型不仅概括了已知的研究结果，而且为未来的研究提供了一个预测可变聚腺苷酸化的方法。最后，我们讨论已知和假设的可变聚腺苷酸化带来的功能。

关键词：基因表达；可变聚腺苷酸化；预测模型；mRNA

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

References

[1] Alkan, S.A., Martincic, K., Milcarek, C., 2006. The hnRNPs F and H2 bind to similar sequences to influence gene expression. Biochem J, 393(1):361-371.

[2] An, J.J., Gharami, K., Liao, G.Y., 2008. Distinct role of long 3′ UTR BDNF mRNA in spine morphology and synaptic plasticity in hippocampal neurons. Cell, 134(1):175-187.

[3] Arhin, G.K., Boots, M., Bagga, P.S., 2002. Downstream sequence elements with different affinities for the hnRNP H/H′ protein influence the processing efficiency of mammalian polyadenylation signals. Nucl Acids Res, 30(8):1842-1850.

[4] Bava, F.A., Eliscovich, C., Ferreira, P.G., 2013. CPEB1 coordinates alternative 3′-UTR formation with translational regulation. Nature, 495(7439):121-125.

[5] Bentley, D.L., 2005. Rules of engagement: co-transcriptional recruitment of pre-mRNA processing factors. Curr Opin Cell Biol, 17(3):251-256.

[6] Boelens, W.C., Jansen, E.J., van Venrooij, W.J., 1993. The human U1 snRNP-specific U1A protein inhibits polyadenylation of its own pre-mRNA. Cell, 72(6):881-892.

[7] Boutet, S.C., Cheung, T.H., Quach, N.L., 2012. Alternative polyadenylation mediates microRNA regulation of muscle stem cell function. Cell Stem Cell, 10(3):327-336.

[8] Brais, B., 2009. Oculopharyngeal muscular dystrophy: a polyalanine myopathy. Curr Neurol Neurosci Rep, 9(1):76-82.

[9] Brown, S.J., Stoilov, P., Xing, Y., 2012. Chromatin and epigenetic regulation of pre-mRNA processing. Hum Mol Genet, 21(R1):R90

[10] Castelo-Branco, P., Furger, A., Wollerton, M., 2004. Polypyrimidine tract binding protein modulates efficiency of polyadenylation. Mol Cell Biol, 24(10):4174-4183.

[11] Chan, S., Choi, E.A., Shi, Y., 2011. Pre-mRNA 3′-end processing complex assembly and function. Wiley Interdiscip Rev RNA, 2(3):321-335.

[12] Chuvpilo, S., Zimmer, M., Kerstan, A., 1999. Alternative polyadenylation events contribute to the induction of NF-ATc in effector T cells. Immunity, 10(2):261-269.

[13] Colgan, D.F., Manley, J.L., 1997. Mechanism and regulation of mRNA polyadenylation. Genes Dev, 11(21):2755-2766.

[14] Cowley, M., Wood, A.J., Bohm, S., 2012. Epigenetic control of alternative mRNA processing at the imprinted Herc3/Nap1l5 locus. Nucl Acids Res, 40(18):8917-8926.

[15] Danckwardt, S., Hentze, M.W., Kulozik, A.E., 2008. 3′ end mRNA processing: molecular mechanisms and implications for health and disease. EMBO J, 27(3):482-498.

[16] Danckwardt, S., Gantzert, A.S., Macher-Goeppinger, S., 2011. p38 MAPK controls prothrombin expression by regulated RNA 3′ end processing. Mol Cell, 41(3):298-310.

[17] de Klerk, E., Venema, A., Anvar, S.Y., 2012. Poly(A) binding protein nuclear 1 levels affect alternative polyadenylation. Nucl Acids Res, 40(18):9089

[18] Denome, R.M., Cole, C.N., 1988. Patterns of polyadenylation site selection in gene constructs containing multiple polyadenylation signals. Mol Cell Biol, 8:4829-4839.

[19] Derti, A., Garrett-Engele, P., Macisaac, K.D., 2012. A quantitative atlas of polyadenylation in five mammals. Genome Res, 22(6):1173-1183.

[20] Dittmar, K.A., Jiang, P., Park, J.W., 2012. Genome-wide determination of a broad ESRP-regulated posttranscriptional network by high-throughput sequencing. Mol Cell Biol, 32(8):1468-1482.

[21] Elkon, R., Drost, J., van Haaften, G., 2012. E2F mediates enhanced alternative polyadenylation in proliferation. Genome Biol, 13(7):R59

[22] Elkon, R., Ugalde, A.P., Agami, R., 2013. Alternative cleavage and polyadenylation: extent, regulation and function. Nat Rev Genet, 14(7):496-506.

[23] Flavell, S.W., Kim, T.K., Gray, J.M., 2008. Genome-wide analysis of MEF2 transcriptional program reveals synaptic target genes and neuronal activity-dependent polyadenylation site selection. Neuron, 60(6):1022-1038.

[24] Fu, Y., Sun, Y., Li, Y., 2011. Differential genome-wide profiling of tandem 3′ UTRs among human breast cancer and normal cells by high-throughput sequencing. Genome Res, 21(5):741-747.

[25] Gawande, B., Robida, M.D., Rahn, A., 2006. Drosophila Sex-lethal protein mediates polyadenylation switching in the female germline. EMBO J, 25(6):1263-1272.

[26] Hirose, Y., Manley, J.L., 2000. RNA polymerase II and the integration of nuclear events. Genes Dev, 14:1415-1429.

[27] Jan, C.H., Friedman, R.C., Ruby, J.G., 2010. Formation, regulation and evolution of Caenorhabditis elegans 3′UTRs. Nature, 469(7328):97-101.

[28] Jenal, M., Elkon, R., Loayza-Puch, F., 2012. The poly(A)-binding protein nuclear 1 suppresses alternative cleavage and polyadenylation sites. Cell, 149(3):538-553.

[29] Ji, X., Wan, J., Vishnu, M., 2013. αCP poly(C) binding proteins act as global regulators of alternative polyadenylation. Mol Cell Biol, 33(13):2560-2573.

[30] Ji, Z., Tian, B., 2009. Reprogramming of 3′ untranslated regions of mRNAs by alternative polyadenylation in generation of pluripotent stem cells from different cell types. PLoS ONE, 4(12):e8419

[31] Ji, Z., Lee, J.Y., Pan, Z., 2009. Progressive lengthening of 3′ untranslated regions of mRNAs by alternative polyadenylation during mouse embryonic development. PNAS, 106(17):7028-7033.

[32] Juge, F., Audibert, A., Benoit, B., 2000. Tissue-specific autoregulation of Drosophila suppressor of forked by alternative poly(A) site utilization leads to accumulation of the suppressor of forked protein in mitotically active cells. RNA, 6(11):1529-1538.

[33] Kleiman, F.E., Manley, J.L., 2001. The BARD1-CstF-50 interaction links mRNA 3′ end formation to DNA damage and tumor suppression. Cell, 104(5):743-753.

[34] Lackford, B., Yao, C., Charles, G.M., 2014. Fip1 regulates mRNA alternative polyadenylation to promote stem cell self-renewal. EMBO J, 33(8):878-889.

[35] Lianoglou, S., Garg, V., Yang, J.L., 2013. Ubiquitously transcribed genes use alternative polyadenylation to achieve tissue-specific expression. Genes Dev, 27(21):2380-2396.

[36] Liao, G.Y., An, J.J., Gharami, K., 2012. Dendritically targeted Bdnf mRNA is essential for energy balance and response to leptin. Nat Med, 18(4):564-571.

[37] Luo, W., Ji, Z., Pan, Z., 2013. The conserved intronic cleavage and polyadenylation site of CstF-77 gene imparts control of 3′ end processing activity through feedback autoregulation and by U1 snRNP. PLoS Genet, 9(7):e1003613

[38] Martin, G., Gruber, A.R., Keller, W., 2012. Genomewide analysis of pre-mrna 3′ end processing reveals a decisive role of human cleavage factor I in the regulation of 3′ UTR length. Cell Rep, 1(6):753-763.

[39] Martincic, K., Campbell, R., Edwalds-Gilbert, G., 1998. Increase in the 64-kDa subunit of the polyadenylation/cleavage stimulatory factor during the G₀ to S phase transition. PNAS, 95(19):11095-11100.

[40] Mayr, C., Bartel, D.P., 2009. Widespread shortening of 3′UTRs by alternative cleavage and polyadenylation activates oncogenes in cancer cells. Cell, 138(4):673-684.

[41] Mueller, A.A., Cheung, T.H., Rando, T.A., 2013. All′s well that ends well: alternative polyadenylation and its implications for stem cell biology. Curr Opin Cell Biol, 25(2):222-232.

[42] Muñoz, M.J., Prez Santangelo, M.S., Paronetto, M.P., 2009. DNA damage regulates alternative splicing through inhibition of RNA polymerase II elongation. Cell, 137(4):708-720.

[43] Ozsolak, F., Kapranov, P., Foissac, S., 2010. Comprehensive polyadenylation site maps in yeast and human reveal pervasive alternative polyadenylation. Cell, 143(6):1018-1029.

[44] Pan, Z., Zhang, H., Hague, L.K., 2006. An intronic polyadenylation site in human and mouse CstF-77 genes suggests an evolutionarily conserved regulatory mechanism. Gene, 366(2):325-334.

[45] Park, J.Y., Li, W., Zheng, D., 2011. Comparative analysis of mRNA isoform expression in cardiac hypertrophy and development reveals multiple post-transcriptional regulatory modules. PLoS ONE, 6(7):e22391

[46] Pinto, P.A., Henriques, T., Freitas, M.O., 2011. RNA polymerase II kinetics in polo polyadenylation signal selection. EMBO J, 30(12):2431-2444.

[47] Proudfoot, N.J., Furger, A., Dye, M.J., 2002. Integrating mRNA processing with transcription. Cell, 108(4):501-512.

[48] Sandberg, R., Neilson, J.R., Sarma, A., 2008. Proliferating cells express mRNAs with shortened 3′ untranslated regions and fewer microRNA target sites. Science, 320(5883):1643-1647.

[49] Shepard, P.J., Choi, E.A., Lu, J., 2011. Complex and dynamic landscape of RNA polyadenylation revealed by PAS-Seq. RNA, 17(4):761-772.

[50] Shi, Y., 2012. Alternative polyadenylation: new insights from global analyses. RNA, 18(12):2105-2117.

[51] Shi, Y., Di Giammartino, D.C., Taylor, D., 2009. Molecular architecture of the human pre-mRNA 3′ processing complex. Mol Cell, 33(3):365-376.

[52] Smibert, P., Miura, P., Westholm, J.O., 2012. Global patterns of tissue-specific alternative polyadenylation in Drosophila . Cell Rep, 1(3):277-289.

[53] Spies, N., Burge, C.B., Bartel, D.P., 2013. 3′ UTR-isoform choice has limited influence on the stability and translational efficiency of most mRNAs in mouse fibroblasts. Genome Res, 23(12):2078-2090.

[54] Takagaki, Y., Manley, J.L., 1998. Levels of polyadenylation factor CstF-64 control IgM heavy chain mRNA accumulation and other events associated with B cell differentiation. Mol Cell, 2(6):761-771.

[55] Takagaki, Y., Seipelt, R.L., Peterson, M.L., 1996. The polyadenylation factor CstF-64 regulates alternative processing of IgM heavy chain pre-mRNA during B cell differentiation. Cell, 87(5):941-952.

[56] Tian, B., Graber, J.H., 2012. Signals for pre-mRNA cleavage and polyadenylation. Wiley Interdiscip Rev RNA, 3(3):385-396.

[57] Tian, B., Manley, J.L., 2013. Alternative cleavage and polyadenylation: the long and short of it. Trends Biochem Sci, 38(6):312

[58] Ulitsky, I., Shkumatava, A., Jan, C.H., 2012. Extensive alternative polyadenylation during zebrafish development. Genome Res, 22(10):2054-2066.

[59] Vagner, S., Ruegsegger, U., Gunderson, S.I., 2000. Position-dependent inhibition of the cleavage step of pre-mRNA 3′-end processing by U1 snRNP. RNA, 6(2):178-188.

[60] Wood, A.J., Schulz, R., Woodfine, K., 2008. Regulation of alternative polyadenylation by genomic imprinting. Genes Dev, 22(9):1141-1146.

[61] Yao, C., Biesinger, J., Wan, J., 2012. Transcriptome-wide analyses of CstF64-RNA interactions in global regulation of mRNA alternative polyadenylation. PNAS, 109(46):18773-18778.

[62] Yao, C., Choi, E.A., Weng, L., 2013. Overlapping and distinct functions of CstF64 and CstF64tau in mammalian mRNA 3′ processing. RNA, 19(12):1781-1790.

[63] Yu, L., Volkert, M.R., 2013. UV damage regulates alternative polyadenylation of the RPB2 gene in yeast. Nucl Acids Res, 41(5):3104-3114.

[64] Zhao, J., Hyman, L., Moore, C., 1999. Formation of mRNA 3′ ends in eukaryotes: mechanism, regulation, and interrelationships with other steps in mRNA synthesis. Microbiol Mol Biol Rev, 63(2):405-445.

Similar articles

- Go to

多腺苷酸化之密码：调解mRNA可变聚腺苷酸化的统一模型

Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article

References