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14. Additional file 2: of QsRNA-seq: a method for high-throughput profiling and quantifying small RNAs

Author

Fishman, Alla, Light, Dean, and Lamm, Ayelet

Abstract

Table S1. Sizes of nucleic acid fragments used and generated during QsRNA-seq library preparation process. Figure S1. Comparing the yield of PAGE-based method versus QsRNA-seq small RNA library preparation methods. Table S2. Comparison between libraries prepared by PAGE-based method and libraries prepared by QsRNA-seq from the same RNA sample. Figure S2. Estimation of ligation and PCR derived biases when adding UMI. Figure S3. Quantity and purity of QsRNA-seq generated libraries. Table S3. Summary of libraries generated in the study. Figure S4. Reducing starting RNA quantity by 10-fold produces similar results. Figure S5. There is a high correlation between samples generated from the same RNA by PAGE-based method and by QsRNA-seq. Figure S6. Variance between collapsed and non-collapsed biological and technical replica samples at C. elegans L4 stage is low. Figure S7. Collapsing sequences using UMI reduces PCR biases. Figure S8. Collapsing sequences using UMI does not change differential expression results of miRNAs. Figure S9. The 26-nt-long sequences primarily start with 5â G. Figure S10. Size distribution of C. elegans sRNA library sequences with and without UMI. Figure S11. Size distribution of C. elegans sRNA library sequences generated by the PAGE-based method or by QsRNA-seq. Figure S12. Size distribution of sequences from human brain sRNA library generated by QsRNA-seq. Figure S13. Size distribution of C. elegans sRNA library sequences generated by QsRNA-seq after phosphatase treatment. Figure S14. The 22-nt-long microRNAs are expressed similarly in C. elegans embryo and L4 stages. (PDF 3458 kb)

Published
2018
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18. Positioning Europe for the EPITRANSCRIPTOMICS challenge

Author

Jantsch, Michael F., primary, Quattrone, Alessandro, additional, O'Connell, Mary, additional, Helm, Mark, additional, Frye, Michaela, additional, Macias-Gonzales, Manuel, additional, Ohman, Marie, additional, Ameres, Stefan, additional, Willems, Luc, additional, Fuks, Francois, additional, Oulas, Anastasis, additional, Vanacova, Stepanka, additional, Nielsen, Henrik, additional, Bousquet-Antonelli, Cecile, additional, Motorin, Yuri, additional, Roignant, Jean-Yves, additional, Balatsos, Nikolaos, additional, Dinnyes, Andras, additional, Baranov, Pavel, additional, Kelly, Vincent, additional, Lamm, Ayelet, additional, Rechavi, Gideon, additional, Pelizzola, Mattia, additional, Liepins, Janis, additional, Holodnuka Kholodnyuk, Irina, additional, Zammit, Vanessa, additional, Ayers, Duncan, additional, Drablos, Finn, additional, Dahl, John Arne, additional, Bujnicki, Janusz, additional, Jeronimo, Carmen, additional, Almeida, Raquel, additional, Neagu, Monica, additional, Costache, Marieta, additional, Bankovic, Jasna, additional, Banovic, Bojana, additional, Kyselovic, Jan, additional, Valor, Luis Miguel, additional, Selbert, Stefan, additional, Pir, Pinar, additional, Demircan, Turan, additional, Cowling, Victoria, additional, Schäfer, Matthias, additional, Rossmanith, Walter, additional, Lafontaine, Denis, additional, David, Alexandre, additional, Carre, Clement, additional, Lyko, Frank, additional, Schaffrath, Raffael, additional, Schwartz, Schraga, additional, Verdel, Andre, additional, Klungland, Arne, additional, Purta, Elzbieta, additional, Timotijevic, Gordana, additional, Cardona, Fernando, additional, Davalos, Alberto, additional, Ballana, Ester, additional, O´Carroll, Donal, additional, Ule, Jernej, additional, and Fray, Rupert, additional

Published
2018
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21. Positioning Europe for the EPITRANSCRIPTOMICS challenge

Author

Jantsch, Michael F., Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Luc, Fuks, Francois, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, Cecile, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Kholodnyuk, Irina Holodnuka, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Banković, Jasna, Banović Đeri, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schaefer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijević, Gordana, Cardona, Fernando, Davalos, Alberto, Ballana, Ester, O'Carroll, Donal, Ule, Jernej, Fray, Rupert, Jantsch, Michael F., Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Luc, Fuks, Francois, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, Cecile, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Kholodnyuk, Irina Holodnuka, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Banković, Jasna, Banović Đeri, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schaefer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijević, Gordana, Cardona, Fernando, Davalos, Alberto, Ballana, Ester, O'Carroll, Donal, Ule, Jernej, and Fray, Rupert

Abstract

The genetic alphabet consists of the four letters: C, A, G, and T in DNA and C,A,G, and U in RNA. Triplets of these four letters jointly encode 20 different amino acids out of which proteins of all organisms are built. This system is universal and is found in all kingdoms of life. However, bases in DNA and RNA can be chemically modified. In DNA, around 10 different modifications are known, and those have been studied intensively over the past 20years. Scientific studies on DNA modifications and proteins that recognize them gave rise to the large field of epigenetic and epigenomic research. The outcome of this intense research field is the discovery that development, ageing, and stem-cell dependent regeneration but also several diseases including cancer are largely controlled by the epigenetic state of cells. Consequently, this research has already led to the first FDA approved drugs that exploit the gained knowledge to combat disease. In recent years, the similar to 150 modifications found in RNA have come to the focus of intense research. Here we provide a perspective on necessary and expected developments in the fast expanding area of RNA modifications, termed epitranscriptomics.

Published
2018

22. Positioning Europe for the EPITRANSCRIPTOMICS challenge

Author

Jantsch, Michael F, Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Luc, Fuks, Francois, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, Cecile, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Holodnuka Kholodnyuk, Irina, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Bankovic, Jasna, Banovic, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schäfer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijevic, Gordana, Cardona, Fernando, Davalos, Alberto, Ballana, Ester, O Carroll, Donal, Ule, Jernej, Fray, Rupert, Jantsch, Michael F, Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Luc, Fuks, Francois, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, Cecile, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Holodnuka Kholodnyuk, Irina, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Bankovic, Jasna, Banovic, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schäfer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijevic, Gordana, Cardona, Fernando, Davalos, Alberto, Ballana, Ester, O Carroll, Donal, Ule, Jernej, and Fray, Rupert

Abstract

The genetic alphabet consists of the four letters: C, A, G, and T in DNA and C,A,G, and U in RNA. Triplets of these four letters jointly encode 20 different amino acids out of which proteins of all organisms are built. This system is universal and is found in all kingdoms of life. However, bases in DNA and RNA can be chemically modified. In DNA, around 10 different modifications are known, and those have been studied intensively over the past 20 years. Scientific studies on DNA modifications and proteins that recognize them gave rise to the large field of epigenetic and epigenomic research. The outcome of this intense research field is the discovery that development, ageing, and stem-cell dependent regeneration but also several diseases including cancer are largely controlled by the epigenetic state of cells. Consequently, this research has already led to the first FDA approved drugs that exploit the gained knowledge to combat disease. In recent years, the ~150 modifications found in RNA have come to the focus of intense research. Here we provide a perspective on necessary and expected developments in the fast expanding area of RNA modifications, termed epitranscriptomics.

Published
2018

23. Positioning Europe for the EPITRANSCRIPTOMICS challenge.

Author

Jantsch, Michael MF, Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Lucas, Fuks, François, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, C, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Holodnuka Kholodnyuk, Irina, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz Marek, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Bankovic, Jasna, Banovic, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schäfer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijevic, Gordana, Cardona, F., Davalos, Alberto, Ballana, Ester, O Carroll, Donal, Ule, Jernej, Fray, Rupert, Jantsch, Michael MF, Quattrone, Alessandro, O'Connell, Mary, Helm, Mark, Frye, Michaela, Macias-Gonzales, Manuel, Ohman, Marie, Ameres, Stefan, Willems, Lucas, Fuks, François, Oulas, Anastasis, Vanacova, Stepanka, Nielsen, Henrik, Bousquet-Antonelli, C, Motorin, Yuri, Roignant, Jean-Yves, Balatsos, Nikolaos, Dinnyes, Andras, Baranov, Pavel, Kelly, Vincent, Lamm, Ayelet, Rechavi, Gideon, Pelizzola, Mattia, Liepins, Janis, Holodnuka Kholodnyuk, Irina, Zammit, Vanessa, Ayers, Duncan, Drablos, Finn, Dahl, John Arne, Bujnicki, Janusz Marek, Jeronimo, Carmen, Almeida, Raquel, Neagu, Monica, Costache, Marieta, Bankovic, Jasna, Banovic, Bojana, Kyselovic, Jan, Valor, Luis Miguel, Selbert, Stefan, Pir, Pinar, Demircan, Turan, Cowling, Victoria, Schäfer, Matthias, Rossmanith, Walter, Lafontaine, Denis, David, Alexandre, Carre, Clement, Lyko, Frank, Schaffrath, Raffael, Schwartz, Schraga, Verdel, Andre, Klungland, Arne, Purta, Elzbieta, Timotijevic, Gordana, Cardona, F., Davalos, Alberto, Ballana, Ester, O Carroll, Donal, Ule, Jernej, and Fray, Rupert

Abstract

The genetic alphabet consists of the four letters: C, A, G, and T in DNA and C,A,G, and U in RNA. Triplets of these four letters jointly encode 20 different amino acids out of which proteins of all organisms are built. This system is universal and is found in all kingdoms of life. However, bases in DNA and RNA can be chemically modified. In DNA, around 10 different modifications are known, and those have been studied intensively over the past 20 years. Scientific studies on DNA modifications and proteins that recognize them gave rise to the large field of epigenetic and epigenomic research. The outcome of this intense research field is the discovery that development, ageing, and stem-cell dependent regeneration but also several diseases including cancer are largely controlled by the epigenetic state of cells. Consequently, this research has already led to the first FDA approved drugs that exploit the gained knowledge to combat disease. In recent years, the ~150 modifications found in RNA have come to the focus of intense research. Here we provide a perspective on necessary and expected developments in the fast expanding area of RNA modifications, termed epitranscriptomics., SCOPUS: no.j, info:eu-repo/semantics/published

Published
2018

32. A-to-I RNA editing promotes developmental stage–specific gene and lncRNA expression

Author

Goldstein, Boaz, Agranat-Tamir, Lily, Light, Dean, Ben-Naim Zgayer, Orna, Fishman, Alla, and Lamm, Ayelet T.

Abstract

A-to-I RNA editing is a conserved widespread phenomenon in which adenosine (A) is converted to inosine (I) by adenosine deaminases (ADARs) in double-stranded RNA regions, mainly noncoding. Mutations in ADAR enzymes in Caenorhabditis eleganscause defects in normal development but are not lethal as in human and mouse. Previous studies in C. elegansindicated competition between RNA interference (RNAi) and RNA editing mechanisms, based on the observation that worms that lack both mechanisms do not exhibit defects, in contrast to the developmental defects observed when only RNA editing is absent. To study the effects of RNA editing on gene expression and function, we established a novel screen that enabled us to identify thousands of RNA editing sites in nonrepetitive regions in the genome. These include dozens of genes that are edited at their 3′ UTR region. We found that these genes are mainly germline and neuronal genes, and that they are down-regulated in the absence of ADAR enzymes. Moreover, we discovered that almost half of these genes are edited in a developmental-specific manner, indicating that RNA editing is a highly regulated process. We found that many pseudogenes and other lncRNAs are also extensively down-regulated in the absence of ADARs in the embryo but not in the fourth larval (L4) stage. This down-regulation is not observed upon additional knockout of RNAi. Furthermore, levels of siRNAs aligned to pseudogenes in ADAR mutants are enhanced. Taken together, our results suggest a role for RNA editing in normal growth and development by regulating silencing via RNAi.

Published
2017
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33. Ce-emerin and LEM-2: essential roles in Caenorhabditis elegansdevelopment, muscle function, and mitosis

Author

Barkan, Rachel, Zahand, Adam J., Sharabi, Kfir, Lamm, Ayelet T., Feinstein, Naomi, Haithcock, Erin, Wilson, Katherine L., Liu, Jun, and Gruenbaum, Yosef

Abstract

Caenorhabditis eleganslacking both Ce-emerin and LEM-2 show that these proteins are essential for development of specific lineages, mitosis in somatic cells, and smooth muscle activity. Reduced life span and smooth muscle activity of LEM-2–null worms predicts human LEM2 gene links to diseases more severe than Emery-Dreifuss muscular dystrophy.

Published
2012
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34. Ce-emerin and LEM-2: essential roles in Caenorhabditis elegans development, muscle function, and mitosis

Author

Barkan, Rachel, Zahand, Adam J., Sharabi, Kfir, Lamm, Ayelet T., Feinstein, Naomi, Haithcock, Erin, Wilson, Katherine L., Liu, Jun, and Gruenbaum, Yosef

Abstract

Emerin and LEM2 are ubiquitous inner nuclear membrane proteins conserved from humans to Caenorhabditis elegans. Loss of human emerin causes Emery-Dreifuss muscular dystrophy (EDMD). To test the roles of emerin and LEM2 in somatic cells, we used null alleles of both genes to generate C. elegans animals that were either hypomorphic (LEM-2–null and heterozygous for Ce-emerin) or null for both proteins. Single-null and hypomorphic animals were viable and fertile. Double-null animals used the maternal pool of Ce-emerin to develop to the larval L2 stage, then arrested. Nondividing somatic cell nuclei appeared normal, whereas dividing cells had abnormal nuclear envelope and chromatin organization and severe defects in postembryonic cell divisions, including the mesodermal lineage. Life span was unaffected by loss of Ce-emerin alone but was significantly reduced in LEM-2–null animals, and double-null animals had an even shorter life span. In addition to striated muscle defects, double-null animals and LEM-2–null animals showed unexpected defects in smooth muscle activity. These findings implicate human LEM2 mutations as a potential cause of EDMD and further suggest human LEM2 mutations might cause distinct disorders of greater severity, since C. elegans lacking only LEM-2 had significantly reduced life span and smooth muscle activity.

Published
2012

35. Disruption in A-to-I Editing Levels Affects C. elegansDevelopment More Than a Complete Lack of Editing

Author

Ganem, Nabeel S., Ben-Asher, Noa, Manning, Aidan C., Deffit, Sarah N., Washburn, Michael C., Wheeler, Emily C., Yeo, Gene W., Zgayer, Orna Ben-Naim, Mantsur, Einav, Hundley, Heather A., and Lamm, Ayelet T.

Abstract

A-to-I RNA editing, catalyzed by ADAR proteins, is widespread in eukaryotic transcriptomes. Studies showed that, in C. elegans, ADR-2 can actively deaminate dsRNA, whereas ADR-1 cannot. Therefore, we set out to study the effect of each of the ADAR genes on the RNA editing process. We performed comprehensive phenotypic, transcriptomics, proteomics, and RNA binding screens on worms mutated in a single ADAR gene. We found that ADR-1 mutants exhibit more-severe phenotypes than ADR-2, and some of them are a result of non-editing functions of ADR-1. We also show that ADR-1 significantly binds edited genes and regulates mRNA expression, whereas the effect on protein levels is minor. In addition, ADR-1 primarily promotes editing by ADR-2 at the L4 stage of development. Our results suggest that ADR-1 has a significant role in the RNA editing process and in altering editing levels that affect RNA expression; loss of ADR-1 results in severe phenotypes.

Published
2019
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36. Multimodal RNA-seq using single-strand, double-strand, and CircLigase-based capture yields a refined and extended description of the C. elegans transcriptome.

Author

Lamm, Ayelet T., Stadler, Michael R., Huibin Zhang, Gent, Jonathan I., and Fire, Andrew Z.

Subjects
*RNA, *GENETICS, *CAENORHABDITIS elegans, *GENOMES, *GENES
Abstract

We have used a combination of three high-throughput RNA capture and sequencing methods to refine and augment the transcriptome map of a well-studied genetic model, Caenorhabditis elegans. The three methods include a standard (non-directional) library preparation protocol relying on cDNA priming and foldback that has been used in several previous studies for transcriptome characterization in this species, and two directional protocols, one involving direct capture of single-stranded RNA fragments and one involving circular-template PCR (CircLigase). We find that each RNA-seq approach shows specific limitations and biases, with the application of multiple methods providing a more complete map than was obtained from any single method. Of particular note in the analysis were substantial advantages of CircLigase-based and ssRNA-based capture for defining sequences and structures of the precise 5' ends (which were lost using the double-strand cDNA capture method). Of the three methods, ssRNA capture was most effective in defining sequences to the poly(A) junction. Using data sets from a spectrum of C. elegans strains and stages and the UCSC Genome Browser, we provide a series of tools, which facilitate rapid visualization and assignment of gene structures. [ABSTRACT FROM AUTHOR]

Published
2011
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37. ADBP-1 regulates ADR-2 nuclear localization to control editing substrate selection.

Author

Eliad B, Schneider N, Zgayer OB, Amichan Y, Glaser F, Erdmann EA, Rajendren S, Hundley HA, and Lamm AT

Abstract

Adenosine-to-inosine (A-to-I) RNA editing, catalyzed by ADAR enzymes, is a prevalent and conserved RNA modification. While A-to-I RNA editing is essential in mammals, in Caenorhabditis elegans , it is not, making them invaluable for RNA editing research. In C. elegans , ADR-2 is the sole catalytic A-to-I editing enzyme, and ADR-1 is an RNA editing regulator. ADAR localization is well-studied in humans but not well-established in C. elegans . In this study, we examine the cellular and tissue-specific localization of ADR-2. We show that while ADR-2 is present in most cells in the embryo, at later developmental stages, its expression is both tissue- and cell-type-specific. Additionally, both ADARs are mainly in the nucleus. ADR-2 is adjacent to the chromosomes during the cell cycle. We show that the nuclear localization of endogenous ADR-2 depends on ADBP-1, not ADR-1. In adbp-1 mutant worms, ADR-2 is mislocalized, while ADR-1 is not, leading to decreased editing levels and de-novo editing, mostly in exons, suggesting that ADR-2 is also functional in the cytoplasm. Besides, mutated ADBP-1 affects gene expression. Furthermore, we show that ADR-2 targets adenosines with different surrounding nucleotides in exons and introns. Our findings indicate that ADR-2 cellular localization is highly regulated and affects its function.

Published
2024
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