CLC number: R4; Q78
On-line Access: 2024-08-27
Received: 2023-10-17
Revision Accepted: 2024-05-08
Crosschecked: 2012-07-19
Cited: 1
Clicked: 5721
Chen Gao, Yibin Wang. Global impact of RNA splicing on transcriptome remodeling in the heart[J]. Journal of Zhejiang University Science B, 2012, 13(8): 603-608.
@article{title="Global impact of RNA splicing on transcriptome remodeling in the heart",
author="Chen Gao, Yibin Wang",
journal="Journal of Zhejiang University Science B",
volume="13",
number="8",
pages="603-608",
year="2012",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B1201006"
}
%0 Journal Article
%T Global impact of RNA splicing on transcriptome remodeling in the heart
%A Chen Gao
%A Yibin Wang
%J Journal of Zhejiang University SCIENCE B
%V 13
%N 8
%P 603-608
%@ 1673-1581
%D 2012
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B1201006
TY - JOUR
T1 - Global impact of RNA splicing on transcriptome remodeling in the heart
A1 - Chen Gao
A1 - Yibin Wang
J0 - Journal of Zhejiang University Science B
VL - 13
IS - 8
SP - 603
EP - 608
%@ 1673-1581
Y1 - 2012
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B1201006
Abstract: In the eukaryotic transcriptome, both the numbers of genes and different RNA species produced by each gene contribute to the overall complexity. These RNA species are generated by the utilization of different transcriptional initiation or termination sites, or more commonly, from different messenger RNA (mRNA) splicing events. Among the 30000+ genes in human genome, it is estimated that more than 95% of them can generate more than one gene product via alternative RNA splicing. The protein products generated from different RNA splicing variants can have different intracellular localization, activity, or tissue-distribution. Therefore, alternative RNA splicing is an important molecular process that contributes to the overall complexity of the genome and the functional specificity and diversity among different cell types. In this review, we will discuss current efforts to unravel the full complexity of the cardiac transcriptome using a deep-sequencing approach, and highlight the potential of this technology to uncover the global impact of RNA splicing on the transcriptome during development and diseases of the heart.
[1]Anders, S., Reyes, A., Huber, W., 2012. Detecting differential usage of exons from RNA-seq data. Genome Res., in press
[2]Asakura, M., Kitakaze, M., 2009. Global gene expression profiling in the failing myocardium. Circ. J., 73(9):1568-1576.
[3]Backs, J., Olson, E.N., 2006. Control of cardiac growth by histone acetylation/deacetylation. Circ. Res., 98(1):15-24.
[4]Barry, S.P., Davidson, S.M., Townsend, P.A., 2008. Molecular regulation of cardiac hypertrophy. Int. J. Biochem. Cell Biol., 40(10):2023-2039.
[5]Bland, C.S., Wang, E.T., Vu, A., David, M.P., Castle, J.C., Johnson, J.M., Burge, C.B., Cooper, T.A., 2010. Global regulation of alternative splicing during myogenic differentiation. Nucleic Acids Res., 38(21):7651-7664.
[6]Buljan, M., Chalancon, G., Eustermann, S., Wagner, G.P., Fuxreiter, M., Bateman, A., Babu, M.M., 2012. Tissue-specific splicing of disordered segments that embed binding motifs rewires protein interaction networks. Mol. Cell, 46(6):871-883.
[7]Chen, M., Manley, J.L., 2009. Mechanisms of alternative splicing regulation: insights from molecular and genomics approaches. Nat. Rev. Mol. Cell Biol., 10(11):741-754.
[8]Concha, M., Wang, X., Cao, S., Baddoo, M., Fewell, C., Lin, Z., Hulme, W., Hedges, D., Mcbride, J., Flemington, E.K., 2012. Identification of new viral genes and transcript isoforms during epstein-barr virus reactivation using RNA-seq. J. Virol., 86(3):1458-1467.
[9]Daines, B., Wang, H., Wang, L., Li, Y., Han, Y., Emmert, D., Gelbart, W., Wang, X., Li, W., Gibbs, R., et al., 2011. The drosophila melanogaster transcriptome by paired-end RNA sequencing. Genome Res., 21(2):315-324.
[10]Dasgupta, T., Ladd, A.N., 2012. The importance of celf control: molecular and biological roles of the CUG-BP, Elav-like family of RNA-binding proteins. Wiley Interdiscip. Rev. RNA, 3(1):104-121.
[11]David, C.J., Chen, M., Assanah, M., Canoll, P., Manley, J.L., 2010. hnRNP proteins controlled by c-Myc deregulate pyruvate kinase mRNA splicing in cancer. Nature, 463(7279):364-368.
[12]de la Grange, P., Gratadou, L., Delord, M., Dutertre, M., Auboeuf, D., 2010. Splicing factor and exon profiling across human tissues. Nucleic Acids Res., 38(9):2825-2838.
[13]Dewey, F.E., Perez, M.V., Wheeler, M.T., Watt, C., Spin, J., Langfelder, P., Horvath, S., Hannenhalli, S., Cappola, T.P., Ashley, E.A., 2011. Gene coexpression network topology of cardiac development, hypertrophy and failure. Circ. Cardiovasc. Genet., 4(1):26-35.
[14]Ding, J.H., Xu, X., Yang, D., Chu, P.H., Dalton, N.D., Ye, Z., Yeakley, J.M., Cheng, H., Xiao, R.P., Ross, J., et al., 2004. Dilated cardiomyopathy caused by tissue-specific ablation of SC35 in the heart. EMBO J., 23(4):885-896.
[15]Edmondson, D.G., Lyons, G.E., Martin, J.F., Olson, E.N., 1994. Mef2 gene expression marks the cardiac and skeletal muscle lineages during mouse embryogenesis. Development, 120(5):1251-1263.
[16]Gang, H., Hai, Y., Dhingra, R., Gordon, J.W., Yurkova, N., Aviv, Y., Li, H., Aguilar, F., Marshall, A., Leygue, E., et al., 2011. A novel hypoxia-inducible spliced variant of mitochondrial death gene Bnip3 promotes survival of ventricular myocytes. Circ. Res., 108(9):1084-1092.
[17]Guo, W., Schafer, S., Greaser, M.L., Radke, M.H., Liss, M., Govindarajan, T., Maatz, H., Schulz, H., Li, S., Parrish, A.M., et al., 2012. RBM20, a gene for hereditary cardiomyopathy, regulates titin splicing. Nat. Med., 18(5):766-773.
[18]Hallegger, M., Llorian, M., Smith, C.W.J., 2010. Alternative splicing: global insights. FEBS J., 277(4):856-866.
[19]Honda, A., Valogne, Y., Bou Nader, M., Brechot, C., Faivre, J., 2012. An intron-retaining splice variant of human cyclin A2, expressed in adult differentiated tissues, induces a g1/s cell cycle arrest in vitro. PLoS One, 7(6):e39249.
[20]Kalsotra, A., Wang, K., Li, P.F., Cooper, T.A., 2010. MicroRNAs coordinate an alternative splicing network during mouse postnatal heart development. Genes Dev., 24(7):653-658.
[21]Koshelev, M., Sarma, S., Price, R.E., Wehrens, X.H.T., Cooper, T.A., 2010. Heart-specific overexpression of CUGBP1 reproduces functional and molecular abnormalities of myotonic dystrophy type 1. Hum. Mol. Genet., 19(6):1066-1075.
[22]Lee, J.H., Gao, C., Peng, G., Greer, C., Ren, S., Wang, Y., Xiao, X., 2011. Analysis of transcriptome complexity through RNA sequencing in normal and failing murine hearts. Circ. Res., 109(12):1332-1341.
[23]Li, G., Bahn, J.H., Lee, J.H., Peng, G., Chen, Z., Nelson, S.F., Xiao, X., 2012. Identification of allele-specific alternative mRNA processing via transcriptome sequencing. Nucleic Acids Res., in press [Epub ahead of print].
[24]Linke, W.A., Bucker, S., 2012. King of hearts: a splicing factor rules cardiac proteins. Nat. Med., 18(5):660-661.
[25]Margulies, K.B., Bednarik, D.P., Dries, D.L., 2009. Genomics, transcriptional profiling, and heart failure. J. Am. Coll. Cardiol., 53(19):1752-1759.
[26]Mcintyre, L., Lopiano, K., Morse, A., Amin, V., Oberg, A., Young, L., Nuzhdin, S., 2011. RNA-seq: technical variability and sampling. BMC Genomics, 12(1):293.
[27]Naya, F.J., Black, B.L., Wu, H., Bassel-Duby, R., Richardson, J.A., Hill, J.A., Olson, E.N., 2002. Mitochondrial deficiency and cardiac sudden death in mice lacking the MEF2A transcription factor. Nat. Med., 8(11):1303-1309.
[28]Ozsolak, F., Milos, P.M., 2011. RNA sequencing: advances, challenges and opportunities. Nat. Rev. Genet., 12(2):87-98.
[29]Pan, Q., Shai, O., Lee, L.J., Frey, B.J., Blencowe, B.J., 2008. Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing. Nat. Genet., 40(12):1413-1415.
[30]Raghavachari, N., Barb, J., Yang, Y., Liu, P., Woodhouse, K., Levy, D., O′Donnell, C., Munson, P.J., Kato, G., 2012. A systematic comparison and evaluation of high density exon arrays and RNA-seq technology used to unravel the peripheral blood transcriptome of sickle cell disease. BMC Med. Genomics, 5(1):28.
[31]Ramchatesingh, J., Zahler, A., Neugebauer, K., Roth, M., Cooper, T., 1995. A subset of SR proteins activates splicing of the cardiac troponin T alternative exon by direct interactions with an exonic enhancer. Mol. Cell. Biol., 15(9):4898-4907.
[32]Refaat, M.M., Lubitz, S.A., Makino, S., Islam, Z., Frangiskakis, J.M., Mehdi, H., Gutmann, R., Zhang, M.L., Bloom, H.L., Macrae, C.A., et al., 2012. Genetic variation in the alternative splicing regulator RBM20 is associated with dilated cardiomyopathy. Heart Rhythm, 9(3):390-396.
[33]Sanchez-Pla, A., Reverter, F., Ruiz de Villa, M.C., Comabella, M., 2012. Transcriptomics: mRNA and alternative splicing. J. Neuroimmunol., 248(1-2):23-31.
[34]Skerjanc, I.S., Petropoulos, H., Ridgeway, A.G., Wilton, S., 1998. Myocyte enhancer factor 2C and Nkx2-5 up-regulate each other’s expression and initiate cardiomyogenesis in P19 cells. J. Biol. Chem., 273(52):34904-34910.
[35]Sultan, M., Schulz, M.H., Richard, H., Magen, A., Klingenhoff, A., Scherf, M., Seifert, M., Borodina, T., Soldatov, A., Parkhomchuk, D., et al., 2008. A global view of gene activity and alternative splicing by deep sequencing of the human transcriptome. Science, 321(5891):956-960.
[36]Wang, E.T., Sandberg, R., Luo, S., Khrebtukova, I., Zhang, L., Mayr, C., Kingsmore, S.F., Schroth, G.P., Burge, C.B., 2008. Alternative isoform regulation in human tissue transcriptomes. Nature, 456(7221):470-476.
[37]Wang, Z., Gerstein, M., Snyder, M., 2009. RNA-seq: a revolutionary tool for transcriptomics. Nat. Rev. Genet., 10(1):57-63.
[38]Warf, M.B., Berglund, J.A., 2007. MBNL binds similar RNA structures in the cug repeats of myotonic dystrophy and its pre-mRNA substrate cardiac troponin T. RNA, 13(12):2238-2251.
[39]Xu, X., Yang, D., Ding, J.H., Wang, W., Chu, P.H., Dalton, N.D., Wang, H.Y., Bermingham, J.R.Jr., Ye, Z., Liu, F., et al., 2005. ASF/SF2-regulated CAMKIIδ alternative splicing temporally reprograms excitation-contraction coupling in cardiac muscle. Cell, 120(1):59-72.
[40]Yae, T., Tsuchihashi, K., Ishimoto, T., Motohara, T., Yoshikawa, M., Yoshida, G.J., Wada, T., Masuko, T., Mogushi, K., Tanaka, H., et al., 2012. Alternative splicing of CD44 mRNA by ESRP1 enhances lung colonization of metastatic cancer cell. Nat. Commun., 3:883.
Open peer comments: Debate/Discuss/Question/Opinion
<1>