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1. Cancer lineage-specific regulation of YAP responsive elements revealed through large-scale functional epigenomic screens

Author

Barbosa, Inês A. M., Gopalakrishnan, Rajaraman, Mercan, Samuele, Mourikis, Thanos P., Martin, Typhaine, Wengert, Simon, Sheng, Caibin, Ji, Fei, Lopes, Rui, Knehr, Judith, Altorfer, Marc, Lindeman, Alicia, Russ, Carsten, Naumann, Ulrike, Golji, Javad, Sprouffske, Kathleen, Barys, Louise, Tordella, Luca, Schübeler, Dirk, Schmelzle, Tobias, and Galli, Giorgio G.

Published
2023
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4. Supplementary Data from CRISPR Screening Identifies Mechanisms of Resistance to KRASG12C and SHP2 Inhibitor Combinations in Non–Small Cell Lung Cancer

Author

Prahallad, Anirudh, primary, Weiss, Andreas, primary, Voshol, Hans, primary, Kerr, Grainne, primary, Sprouffske, Kathleen, primary, Yuan, Tina, primary, Ruddy, David, primary, Meistertzheim, Morgane, primary, Kazic-Legueux, Malika, primary, Kottarathil, Tina, primary, Piquet, Michelle, primary, Cao, Yichen, primary, Martinuzzi-Duboc, Laetitia, primary, Buhles, Alexandra, primary, Adler, Flavia, primary, Mannino, Salvatore, primary, Tordella, Luca, primary, Sansregret, Laurent, primary, Maira, Sauveur-Michel, primary, Graus Porta, Diana, primary, Fedele, Carmine, primary, and Brachmann, Saskia M., primary

Published
2023
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5. CRISPR Screening Identifies Mechanisms of Resistance to KRASG12C and SHP2 Inhibitor Combinations in Non–Small Cell Lung Cancer

Author

Prahallad, Anirudh, primary, Weiss, Andreas, additional, Voshol, Hans, additional, Kerr, Grainne, additional, Sprouffske, Kathleen, additional, Yuan, Tina, additional, Ruddy, David, additional, Meistertzheim, Morgane, additional, Kazic-Legueux, Malika, additional, Kottarathil, Tina, additional, Piquet, Michelle, additional, Cao, Yichen, additional, Martinuzzi-Duboc, Laetitia, additional, Buhles, Alexandra, additional, Adler, Flavia, additional, Mannino, Salvatore, additional, Tordella, Luca, additional, Sansregret, Laurent, additional, Maira, Sauveur-Michel, additional, Graus Porta, Diana, additional, Fedele, Carmine, additional, and Brachmann, Saskia M., additional

Published
2023
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6. Supplemental Figure S6 from Expressed Barcoding Enables High-Resolution Tracking of the Evolution of Drug Tolerance

Author

Cotton, Jennifer L., primary, Estrada Diez, Javier, primary, Sagar, Vivek, primary, Chen, Julie, primary, Piquet, Michelle, primary, Alford, John, primary, Song, Youngchul, primary, Li, Xiaoyan, primary, Riester, Markus, primary, DiMare, Matthew T., primary, Schumacher, Katja, primary, Boulay, Gaylor, primary, Sprouffske, Kathleen, primary, Fan, Lin, primary, Burks, Tyler, primary, Mansur, Leandra, primary, Wagner, Joel, primary, Bhang, Hyo-eun C., primary, Iartchouk, Oleg, primary, Reece-Hoyes, John, primary, Morris, Erick J., primary, Hammerman, Peter S., primary, Ruddy, David A., primary, Korn, Joshua M., primary, Engelman, Jeffrey A., primary, and Niederst, Matthew J., primary

Published
2023
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7. Data from Expressed Barcoding Enables High-Resolution Tracking of the Evolution of Drug Tolerance

Author

Cotton, Jennifer L., primary, Estrada Diez, Javier, primary, Sagar, Vivek, primary, Chen, Julie, primary, Piquet, Michelle, primary, Alford, John, primary, Song, Youngchul, primary, Li, Xiaoyan, primary, Riester, Markus, primary, DiMare, Matthew T., primary, Schumacher, Katja, primary, Boulay, Gaylor, primary, Sprouffske, Kathleen, primary, Fan, Lin, primary, Burks, Tyler, primary, Mansur, Leandra, primary, Wagner, Joel, primary, Bhang, Hyo-eun C., primary, Iartchouk, Oleg, primary, Reece-Hoyes, John, primary, Morris, Erick J., primary, Hammerman, Peter S., primary, Ruddy, David A., primary, Korn, Joshua M., primary, Engelman, Jeffrey A., primary, and Niederst, Matthew J., primary

Published
2023
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8. Supplemental Figure and Table Legends from Expressed Barcoding Enables High-Resolution Tracking of the Evolution of Drug Tolerance

Author

Cotton, Jennifer L., primary, Estrada Diez, Javier, primary, Sagar, Vivek, primary, Chen, Julie, primary, Piquet, Michelle, primary, Alford, John, primary, Song, Youngchul, primary, Li, Xiaoyan, primary, Riester, Markus, primary, DiMare, Matthew T., primary, Schumacher, Katja, primary, Boulay, Gaylor, primary, Sprouffske, Kathleen, primary, Fan, Lin, primary, Burks, Tyler, primary, Mansur, Leandra, primary, Wagner, Joel, primary, Bhang, Hyo-eun C., primary, Iartchouk, Oleg, primary, Reece-Hoyes, John, primary, Morris, Erick J., primary, Hammerman, Peter S., primary, Ruddy, David A., primary, Korn, Joshua M., primary, Engelman, Jeffrey A., primary, and Niederst, Matthew J., primary

Published
2023
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9. Supplemental Tables 1 - 12 from Expressed Barcoding Enables High-Resolution Tracking of the Evolution of Drug Tolerance

Author

Cotton, Jennifer L., primary, Estrada Diez, Javier, primary, Sagar, Vivek, primary, Chen, Julie, primary, Piquet, Michelle, primary, Alford, John, primary, Song, Youngchul, primary, Li, Xiaoyan, primary, Riester, Markus, primary, DiMare, Matthew T., primary, Schumacher, Katja, primary, Boulay, Gaylor, primary, Sprouffske, Kathleen, primary, Fan, Lin, primary, Burks, Tyler, primary, Mansur, Leandra, primary, Wagner, Joel, primary, Bhang, Hyo-eun C., primary, Iartchouk, Oleg, primary, Reece-Hoyes, John, primary, Morris, Erick J., primary, Hammerman, Peter S., primary, Ruddy, David A., primary, Korn, Joshua M., primary, Engelman, Jeffrey A., primary, and Niederst, Matthew J., primary

Published
2023
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10. Expressed Barcoding Enables High-Resolution Tracking of the Evolution of Drug Tolerance

Author

Cotton, Jennifer L., primary, Estrada Diez, Javier, additional, Sagar, Vivek, additional, Chen, Julie, additional, Piquet, Michelle, additional, Alford, John, additional, Song, Youngchul, additional, Li, Xiaoyan, additional, Riester, Markus, additional, DiMare, Matthew T., additional, Schumacher, Katja, additional, Boulay, Gaylor, additional, Sprouffske, Kathleen, additional, Fan, Lin, additional, Burks, Tyler, additional, Mansur, Leandra, additional, Wagner, Joel, additional, Bhang, Hyo-eun C., additional, Iartchouk, Oleg, additional, Reece-Hoyes, John, additional, Morris, Erick J., additional, Hammerman, Peter S., additional, Ruddy, David A., additional, Korn, Joshua M., additional, Engelman, Jeffrey A., additional, and Niederst, Matthew J., additional

Published
2023
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11. Supplementary Tables from The Discovery of SWI/SNF Chromatin Remodeling Activity as a Novel and Targetable Dependency in Uveal Melanoma

Author

Rago, Florencia, primary, Elliott, GiNell, primary, Li, Ailing, primary, Sprouffske, Kathleen, primary, Kerr, Grainne, primary, Desplat, Aurore, primary, Abramowski, Dorothee, primary, Chen, Julie T., primary, Farsidjani, Ali, primary, Xiang, Kay X., primary, Bushold, Geoffrey, primary, Feng, Yun, primary, Shirley, Matthew D., primary, Bric, Anka, primary, Vattay, Anthony, primary, Möbitz, Henrik, primary, Nakajima, Katsumasa, primary, Adair, Christopher D., primary, Mathieu, Simon, primary, Ntaganda, Rukundo, primary, Smith, Troy, primary, Papillon, Julien P.N., primary, Kauffmann, Audrey, primary, Ruddy, David A., primary, Bhang, Hyo-eun C., primary, Castelletti, Deborah, primary, and Jagani, Zainab, primary

Published
2023
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12. Supplementary Figures from The Discovery of SWI/SNF Chromatin Remodeling Activity as a Novel and Targetable Dependency in Uveal Melanoma

Author

Rago, Florencia, primary, Elliott, GiNell, primary, Li, Ailing, primary, Sprouffske, Kathleen, primary, Kerr, Grainne, primary, Desplat, Aurore, primary, Abramowski, Dorothee, primary, Chen, Julie T., primary, Farsidjani, Ali, primary, Xiang, Kay X., primary, Bushold, Geoffrey, primary, Feng, Yun, primary, Shirley, Matthew D., primary, Bric, Anka, primary, Vattay, Anthony, primary, Möbitz, Henrik, primary, Nakajima, Katsumasa, primary, Adair, Christopher D., primary, Mathieu, Simon, primary, Ntaganda, Rukundo, primary, Smith, Troy, primary, Papillon, Julien P.N., primary, Kauffmann, Audrey, primary, Ruddy, David A., primary, Bhang, Hyo-eun C., primary, Castelletti, Deborah, primary, and Jagani, Zainab, primary

Published
2023
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13. Supplementary Data from Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia

Author

Rago, Florencia, primary, Rodrigues, Lindsey Ulkus, primary, Bonney, Megan, primary, Sprouffske, Kathleen, primary, Kurth, Esther, primary, Elliott, GiNell, primary, Ambrose, Jessi, primary, Aspesi, Peter, primary, Oborski, Justin, primary, Chen, Julie T., primary, McDonald, E. Robert, primary, Mapa, Felipa A., primary, Ruddy, David A., primary, Kauffmann, Audrey, primary, Abrams, Tinya, primary, Bhang, Hyo-eun C., primary, and Jagani, Zainab, primary

Published
2023
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14. Data from Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia

Author

Rago, Florencia, primary, Rodrigues, Lindsey Ulkus, primary, Bonney, Megan, primary, Sprouffske, Kathleen, primary, Kurth, Esther, primary, Elliott, GiNell, primary, Ambrose, Jessi, primary, Aspesi, Peter, primary, Oborski, Justin, primary, Chen, Julie T., primary, McDonald, E. Robert, primary, Mapa, Felipa A., primary, Ruddy, David A., primary, Kauffmann, Audrey, primary, Abrams, Tinya, primary, Bhang, Hyo-eun C., primary, and Jagani, Zainab, primary

Published
2023
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16. Supplementary Methods from The Discovery of SWI/SNF Chromatin Remodeling Activity as a Novel and Targetable Dependency in Uveal Melanoma

Author

Rago, Florencia, primary, Elliott, GiNell, primary, Li, Ailing, primary, Sprouffske, Kathleen, primary, Kerr, Grainne, primary, Desplat, Aurore, primary, Abramowski, Dorothee, primary, Chen, Julie T., primary, Farsidjani, Ali, primary, Xiang, Kay X., primary, Bushold, Geoffrey, primary, Feng, Yun, primary, Shirley, Matthew D., primary, Bric, Anka, primary, Vattay, Anthony, primary, Möbitz, Henrik, primary, Nakajima, Katsumasa, primary, Adair, Christopher D., primary, Mathieu, Simon, primary, Ntaganda, Rukundo, primary, Smith, Troy, primary, Papillon, Julien P.N., primary, Kauffmann, Audrey, primary, Ruddy, David A., primary, Bhang, Hyo-eun C., primary, Castelletti, Deborah, primary, and Jagani, Zainab, primary

Published
2023
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18. Data from The Discovery of SWI/SNF Chromatin Remodeling Activity as a Novel and Targetable Dependency in Uveal Melanoma

Author

Rago, Florencia, primary, Elliott, GiNell, primary, Li, Ailing, primary, Sprouffske, Kathleen, primary, Kerr, Grainne, primary, Desplat, Aurore, primary, Abramowski, Dorothee, primary, Chen, Julie T., primary, Farsidjani, Ali, primary, Xiang, Kay X., primary, Bushold, Geoffrey, primary, Feng, Yun, primary, Shirley, Matthew D., primary, Bric, Anka, primary, Vattay, Anthony, primary, Möbitz, Henrik, primary, Nakajima, Katsumasa, primary, Adair, Christopher D., primary, Mathieu, Simon, primary, Ntaganda, Rukundo, primary, Smith, Troy, primary, Papillon, Julien P.N., primary, Kauffmann, Audrey, primary, Ruddy, David A., primary, Bhang, Hyo-eun C., primary, Castelletti, Deborah, primary, and Jagani, Zainab, primary

Published
2023
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19. Protein destabilization underlies pathogenic missense mutations in ARID1B

Author

Mermet-Meillon, Fanny, Mercan, Samuele, Bauer-Probst, Beatrice, Allard, Cyril, Bleu, Melusine, Calkins, Keith, Knehr, Judith, Altorfer, Marc, Naumann, Ulrike, Sprouffske, Kathleen, Barys, Louise, Sesterhenn, Fabian, and Galli, Giorgio G.

Abstract

ARID1B is a SWI/SNF subunit frequently mutated in human Coffin–Siris syndrome (CSS) and it is necessary for proliferation of ARID1Amutant cancers. While most CSS ARID1Baberrations introduce frameshifts or stop codons, the functional consequence of missense mutations found in ARID1Bis unclear. We here perform saturated mutagenesis screens on ARID1B and demonstrate that protein destabilization is the main mechanism associated with pathogenic missense mutations in patients with Coffin–Siris Syndrome.

Published
2024
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23. List of Contributors

Author

Abadie, Jerôme, primary, Ammerpohl, Ole, additional, Arnal, Audrey, additional, Banach, Maureen, additional, Beckmann, Christa, additional, Bernex, Florence, additional, Boddy, Amy M., additional, Brown, Joel S., additional, Brown, Sam P., additional, De Jesús Andino, Francisco, additional, DeGregori, James, additional, Edholm, Eva-Stina, additional, Enriquez-Navas, Pedro M., additional, Ewald, Paul W., additional, Faugère, Dominique, additional, Foo, Jasmine, additional, Garcia, Déborah, additional, Garvey, Colleen M., additional, Gatenby, Robert A., additional, Gidoin, Cindy, additional, Gillies, Robert J., additional, Grunau, Christoph, additional, Harris, Valerie K., additional, Hattermann, Kirsten, additional, Held-Feindt, Janka, additional, Heng, Henry H., additional, Ibrahim-Hashim, Arig, additional, Kareva, Irina, additional, Kokko, Hanna, additional, Labrut, Sophie, additional, Lemberger, Karin, additional, Lindsay, Danika, additional, Lloyd, Mark C., additional, Møller, Anders Pape, additional, Madsen, Thomas, additional, Marusyk, Andriy, additional, McDonald, John F., additional, Mumenthaler, Shannon M., additional, Nedelcu, Aurora M., additional, Nesse, Randolph M., additional, Nunney, Leonard, additional, Read, Andrew F., additional, Rhoo, Kun Hyoe, additional, Röcken, Christoph, additional, Robert, Jacques, additional, Roche, Benjamin, additional, Russell, Shonagh, additional, Schäfer, Heiner, additional, Schem, Christian, additional, Schewe, Denis, additional, Schiffman, Joshua D., additional, Schindler, Susanne, additional, Schulenburg, Hinrich, additional, Sebens, Susanne, additional, Sprouffske, Kathleen, additional, Swain Ewald, Holly A., additional, Synowitz, Michael, additional, Tasiemski, Aurélie, additional, Thomas, Frédéric, additional, Tiwari, Sanjay, additional, Traulsen, Arne, additional, Trauzold, Anna, additional, Ujvari, Beata, additional, Valerius, Thomas, additional, Vincent, Mark, additional, Vittecoq, Marion, additional, Waldetoft, Kristofer Wollein, additional, and Wesch, Daniela, additional

Published
2017
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25. Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia

Author

Rago, Florencia, primary, Rodrigues, Lindsey Ulkus, additional, Bonney, Megan, additional, Sprouffske, Kathleen, additional, Kurth, Esther, additional, Elliott, GiNell, additional, Ambrose, Jessi, additional, Aspesi, Peter, additional, Oborski, Justin, additional, Chen, Julie T., additional, McDonald, E. Robert, additional, Mapa, Felipa A., additional, Ruddy, David A., additional, Kauffmann, Audrey, additional, Abrams, Tinya, additional, Bhang, Hyo-eun C., additional, and Jagani, Zainab, additional

Published
2022
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26. Systematic dissection of transcriptional regulatory networks by genome-scale and single-cell CRISPR screens

Author

Lopes, Rui, primary, Sprouffske, Kathleen, additional, Sheng, Caibin, additional, Uijttewaal, Esther C. H., additional, Wesdorp, Adriana Emma, additional, Dahinden, Jan, additional, Wengert, Simon, additional, Diaz-Miyar, Juan, additional, Yildiz, Umut, additional, Bleu, Melusine, additional, Apfel, Verena, additional, Mermet-Meillon, Fanny, additional, Krese, Rok, additional, Eder, Mathias, additional, Olsen, André Vidas, additional, Hoppe, Philipp, additional, Knehr, Judith, additional, Carbone, Walter, additional, Cuttat, Rachel, additional, Waldt, Annick, additional, Altorfer, Marc, additional, Naumann, Ulrike, additional, Weischenfeldt, Joachim, additional, deWeck, Antoine, additional, Kauffmann, Audrey, additional, Roma, Guglielmo, additional, Schübeler, Dirk, additional, and Galli, Giorgio G., additional

Published
2021
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27. Systematic dissection of transcriptional regulatory networks by genome-scale and single-cell CRISPR screens

Author

Lopes, Rui, Sprouffske, Kathleen, Sheng, Caibin, Uijttewaal, Esther C.H., Wesdorp, Adriana Emma, Dahinden, Jan, Wengert, Simon, Diaz-Miyar, Juan, Yildiz, Umut, Bleu, Melusine, Apfel, Verena, Mermet-Meillon, Fanny, Krese, Rok, Eder, Mathias, Olsen, André Vidas, Hoppe, Philipp, Knehr, Judith, Carbone, Walter, Cuttat, Rachel, Waldt, Annick, Altorfer, Marc, Naumann, Ulrike, Weischenfeldt, Joachim, deWeck, Antoine, Kauffmann, Audrey, Roma, Guglielmo, Schübeler, Dirk, Galli, Giorgio G., Lopes, Rui, Sprouffske, Kathleen, Sheng, Caibin, Uijttewaal, Esther C.H., Wesdorp, Adriana Emma, Dahinden, Jan, Wengert, Simon, Diaz-Miyar, Juan, Yildiz, Umut, Bleu, Melusine, Apfel, Verena, Mermet-Meillon, Fanny, Krese, Rok, Eder, Mathias, Olsen, André Vidas, Hoppe, Philipp, Knehr, Judith, Carbone, Walter, Cuttat, Rachel, Waldt, Annick, Altorfer, Marc, Naumann, Ulrike, Weischenfeldt, Joachim, deWeck, Antoine, Kauffmann, Audrey, Roma, Guglielmo, Schübeler, Dirk, and Galli, Giorgio G.

Abstract

Millions of putative transcriptional regulatory elements (TREs) have been cataloged in the human genome, yet their functional relevance in specific pathophysiological settings remains to be determined. This is critical to understand how oncogenic transcription factors (TFs) engage specific TREs to impose transcriptional programs underlying malignant phenotypes. Here, we combine cutting edge CRISPR screens and epigenomic profiling to functionally survey ≈ 15,000 TREs engaged by estrogen receptor (ER). We show that ER exerts its oncogenic role in breast cancer by engaging TREs enriched in GATA3, TFAP2C, and H3K27Ac signal. These TREs control critical downstream TFs, among which TFAP2C plays an essential role in ER-driven cell proliferation. Together, our work reveals novel insights into a critical oncogenic transcription program and provides a framework to map regulatory networks, enabling to dissect the function of the noncoding genome of cancer cells.

Published
2021

28. Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia

Author

Rago, Florencia, primary, Rodrigues, Lindsey Ulkus, additional, Bonney, Megan, additional, Sprouffske, Kathleen, additional, Kurth, Esther, additional, Elliott, GiNell, additional, Ambrose, Jessi, additional, Aspesi, Peter, additional, Oborski, Justin, additional, Chen, Julie T., additional, McDonald, E. Robert, additional, Mapa, Felipa A, additional, Ruddy, David A., additional, Kauffmann, Audrey, additional, Abrams, Tinya, additional, Bhang, Hyo-eun C., additional, and Jagani, Zainab, additional

Published
2021
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29. Abstract PO-100: Expressed molecular barcoding coupled with single cell RNAseq enables a high resolution investigation into the evolution of drug tolerance

Author

Cotton, Jennifer L., primary, Radhakrishna, Viveksagar Krisnamurthy, additional, Diez, Javier Estrada, additional, Ruddy, David A., additional, Sprouffske, Kathleen, additional, Boulay, Gaylor, additional, Piquet, Michelle, additional, Wagner, Joel, additional, Song, Youngchul, additional, Li, Xiaoyan, additional, Schumacher, Katja, additional, Korn, Joshua, additional, Morris, Erick J., additional, Hammerman, Peter S., additional, Engelman, Jeffrey A., additional, and Niederst, Matthew J., additional

Published
2020
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31. The Discovery of SWI/SNF Chromatin Remodeling Activity as a Novel and Targetable Dependency in Uveal Melanoma

Author

Rago, Florencia, primary, Elliott, GiNell, additional, Li, Ailing, additional, Sprouffske, Kathleen, additional, Kerr, Grainne, additional, Desplat, Aurore, additional, Abramowski, Dorothee, additional, Chen, Julie T., additional, Farsidjani, Ali, additional, Xiang, Kay X., additional, Bushold, Geoffrey, additional, Feng, Yun, additional, Shirley, Matthew D., additional, Bric, Anka, additional, Vattay, Anthony, additional, Möbitz, Henrik, additional, Nakajima, Katsumasa, additional, Adair, Christopher D., additional, Mathieu, Simon, additional, Ntaganda, Rukundo, additional, Smith, Troy, additional, Papillon, Julien P.N., additional, Kauffmann, Audrey, additional, Ruddy, David A., additional, Bhang, Hyo-eun C., additional, Castelletti, Deborah, additional, and Jagani, Zainab, additional

Published
2020
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32. Application of simultaneous selective pressures slows adaptation

Author

Merlo, Lauren M. F., primary, Sprouffske, Kathleen, additional, Howard, Taylor C., additional, Gardiner, Kristin L., additional, Caulin, Aleah F., additional, Blum, Steven M., additional, Evans, Perry, additional, Bedalov, Antonio, additional, Sniegowski, Paul D., additional, and Maley, Carlo C., additional

Published
2020
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33. Abstract A122: Molecular barcoding and single cell approaches to investigate drug tolerance in EGFRmutNSCLC

Author

Cotton, Jennifer L., primary, KrishnamurthyRadhakrishna, Viveksagar, additional, Chen, Julie, additional, Piquet, Michelle, additional, Wagner, Joel, additional, Boulay, Gaylor, additional, Sprouffske, Kathleen, additional, Song, Youngchul, additional, Li, Xiaoyan, additional, Schumacher, Katja, additional, Thierry, Raphael, additional, Kirkpatrick, Nathaniel D., additional, Ruddy, David A., additional, Korn, Joshua, additional, Morris, Erick J., additional, Hammerman, Peter S., additional, Engelman, Jeffrey A., additional, and Niederst, Matthew J., additional

Published
2019
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34. Additional file 21: of Assessing the benefits of horizontal gene transfer by laboratory evolution and genome sequencing

Author

Chu, Hoi, Sprouffske, Kathleen, and Wagner, Andreas

Abstract

Table S14. Summary of growth parameters of butyric acid-evolved clones. We randomly selected four clones from each butyric acid-evolved population (Methods) and measured the clonesâ growth in butyric acid-supplemented liquid media. The mean and standard deviations of growth rate, carrying capacity and area under the growth curve estimated by Growthcurver v0.2.1 are summarized for three replicate measurements and rounded to three significant figures. (DOCX 17Â kb)

Published
2018
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35. Additional file 8: of Assessing the benefits of horizontal gene transfer by laboratory evolution and genome sequencing

Author

Chu, Hoi, Sprouffske, Kathleen, and Wagner, Andreas

Abstract

Table S7. Statistical tests conducted. df: degrees of freedom, n = number of samples. * Statistical test adopted from [103], methods S1. The Mann-Whitney U-test is computed using the package exactRankTests [104] in R. ' Re c Y X $$ \operatorname{Re}{\mathrm{c}}_{\mathrm{Y}}^{\mathrm{X}} $$ ' denotes a population of Y recipient strains exposed to donor strain X. (DOCX 21 kb)

Published
2018
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36. Additional file 30: of Assessing the benefits of horizontal gene transfer by laboratory evolution and genome sequencing

Author

Chu, Hoi, Sprouffske, Kathleen, and Wagner, Andreas

Subjects
endocrine system
Abstract

Table S11. Summary of growth parameters of populations evolved in HPA. The table shows mean and standard deviations of growth rate, carrying capacity and area under the growth curve estimated by Growthcurver v0.2.1 at the end of the HPA-adaptation experiment based on three replicate measurements of growth in HPA-supplemented liquid medium and rounded to three significant digits. (DOCX 14Â kb)

Published
2018
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38. Additional file 9: of Assessing the benefits of horizontal gene transfer by laboratory evolution and genome sequencing

Author

Chu, Hoi, Sprouffske, Kathleen, and Wagner, Andreas

Subjects
endocrine system
Abstract

Table S12. Summary of growth parameters of HPA-evolved clones. We randomly selected four clones from each HPA-evolved population (Methods) and measured the clonesâ growth in HPA-supplemented liquid media. The mean and standard deviations of growth rate, carrying capacity and area under the growth curve estimated by Growthcurver v0.2.1 are summarized for three replicate measurements and rounded to three significant digits. (DOCX 18Â kb)

Published
2018
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39. High mutation rates limit evolutionary adaptation in Escherichia coli

Author

Matic, Ivan, Matic, I ( Ivan ), Sprouffske, Kathleen; https://orcid.org/0000-0001-7081-2598, Aguilar-Rodríguez, José; https://orcid.org/0000-0001-7622-5482, Sniegowski, Paul; https://orcid.org/0000-0003-2788-3192, Wagner, Andreas; https://orcid.org/0000-0003-4299-3840, Matic, Ivan, Matic, I ( Ivan ), Sprouffske, Kathleen; https://orcid.org/0000-0001-7081-2598, Aguilar-Rodríguez, José; https://orcid.org/0000-0001-7622-5482, Sniegowski, Paul; https://orcid.org/0000-0003-2788-3192, and Wagner, Andreas; https://orcid.org/0000-0003-4299-3840

Abstract

Mutation is fundamental to evolution, because it generates the genetic variation on which selection can act. In nature, genetic changes often increase the mutation rate in systems that range from viruses and bacteria to human tumors. Such an increase promotes the accumulation of frequent deleterious or neutral alleles, but it can also increase the chances that a population acquires rare beneficial alleles. Here, we study how up to 100-fold increases in Escherichia coli’s genomic mutation rate affect adaptive evolution. To do so, we evolved multiple replicate populations of asexual E. coli strains engineered to have four different mutation rates for 3000 generations in the laboratory. We measured the ability of evolved populations to grow in their original environment and in more than 90 novel chemical environments. In addition, we subjected the populations to whole genome population sequencing. Although populations with higher mutation rates accumulated greater genetic diversity, this diversity conveyed benefits only for modestly increased mutation rates, where populations adapted faster and also thrived better than their ancestors in some novel environments. In contrast, some populations at the highest mutation rates showed reduced adaptation during evolution, and failed to thrive in all of the 90 alternative environments. In addition, they experienced a dramatic decrease in mutation rate. Our work demonstrates that the mutation rate changes the global balance between deleterious and beneficial mutational effects on fitness. In contrast to most theoretical models, our experiments suggest that this tipping point already occurs at the modest mutation rates that are found in the wild.

Published
2018

41. Searching for a Cancer-Proof Organism: It’s the Journey That Teaches You About the Destination

Author

Ujvari, B., Roche, B., Thomas, F., Ujvari, B ( B. ), Roche, B ( B. ), Thomas, F ( F. ), Kokko, Hanna, Schindler, Susanne, Sprouffske, Kathleen, Ujvari, B., Roche, B., Thomas, F., Ujvari, B ( B. ), Roche, B ( B. ), Thomas, F ( F. ), Kokko, Hanna, Schindler, Susanne, and Sprouffske, Kathleen

Abstract

Despite an obvious focus of cancer as a medical phenomenon affecting human lifespan, cancer occurs across multicellular life. We argue that cancer research could benefit from moving from considering other species’ cancers as mere models of those of humans to embracing the differences across species, as these dictate the logic of natural selection and its ability to “see” cancer as a relevant problem in an organism’s ecology and life history. Simultaneously, cancer should be incorporated more strongly in evolutionary thinking itself. At the origin of multicellularity, there is a gray zone between offspring production and cancer, and the association between sexual reproduction and a unicellular stage in a metazoan life history could prove interesting in this context. The idea that links sex with possibilities to discard “faulty” products of cell divisions is particularly clear in a basal metazoan, the hydra. In larger species with clearly differentiated tissues, there is much to gain from investigating the coevolution of senescence and cancer robustness: prolonging the lifespan of cell lineages (e.g., via telomerase) can be counterproductive for the lifespan of the entire organism, and organisms that live long and are now miniaturized compared with their ancestors (such as birds) should show great promise as study species.

Published
2017

42. Effect of population size and mutation rate on the evolution of RNA sequences on an adaptive landscape determined by RNA folding

Author

Vahdati, Ali R, Sprouffske, Kathleen, Wagner, Andreas, Vahdati, Ali R, Sprouffske, Kathleen, and Wagner, Andreas

Abstract

The dynamics of populations evolving on an adaptive landscape depends on multiple factors, including the structure of the landscape, the rate of mutations, and effective population size. Existing theoretical work often makes ad hoc and simplifying assumptions about landscape structure, whereas experimental work can vary important parameters only to a limited extent. We here overcome some of these limitations by simulating the adaptive evolution of RNA molecules, whose fitness is determined by the thermodynamics of RNA secondary structure folding. We study the influence of mutation rates and population sizes on final mean population fitness, on the substitution rates of mutations, and on population diversity. We show that evolutionary dynamics cannot be understood as a function of mutation rate µ, population size N, or population mutation rate Nµ alone. For example, at a given mutation rate, clonal interference prevents the fixation of beneficial mutations as population size increases, but larger populations still arrive at a higher mean fitness. In addition, at the highest population mutation rates we study, mean final fitness increases with population size, because small populations are driven to low fitness by the relatively higher incidence of mutations they experience. Our observations show that mutation rate and population size can interact in complex ways to influence the adaptive dynamics of a population on a biophysically motivated fitness landscape.

Published
2017

44. Growthcurver: an R package for obtaining interpretable metrics from microbial growth curves

Author

Sprouffske, Kathleen, Wagner, Andreas, Sprouffske, Kathleen, and Wagner, Andreas

Abstract

BACKGROUND: Plate readers can measure the growth curves of many microbial strains in a high-throughput fashion. The hundreds of absorbance readings collected simultaneously for hundreds of samples create technical hurdles for data analysis. RESULTS: Growthcurver summarizes the growth characteristics of microbial growth curve experiments conducted in a plate reader. The data are fitted to a standard form of the logistic equation, and the parameters have clear interpretations on population-level characteristics, like doubling time, carrying capacity, and growth rate. CONCLUSIONS: Growthcurver is an easy-to-use R package available for installation from the Comprehensive R Archive Network (CRAN). The source code is available under the GNU General Public License and can be obtained from Github (Sprouffske K, Growthcurver sourcecode, 2016).

Published
2016

49. Modeling the evolutionary and differentiation dynamics of neoplastic progression

Author

Sprouffske, Kathleen and Sprouffske, Kathleen

Abstract

Cancer is an evolutionary system that results from the accumulation of somatic mutations, many of which are thought to increase somatic fitness of cells by allowing them to divide faster, die less frequently, or ignore the rules dictated by their environments. New mutations in individual cells within a neoplasm can create subclones of genetically identical cells all sharing a common ancestor, and these subclones can then compete with each other for limited resources. We consider somatic evolution in two contexts: the progression of normal cell populations to cancer cell populations, and the dynamics of evolution within cancer cell populations. Additionally, human tissues are subdivided into populations with varying levels of proliferative potential. In this context, stem cells are thought to divide symmetrically to replenish their numbers and asymmetrically to generate the transient cells which in turn generate the terminally differentiated cells that make up the bulk of the tissue and perform their tissue specific roles; transient cells can divide multiple times, becoming progressively more differentiated. This architecture of differentiation minimizes the accumulation of mutations; tissues in which disruptions to the forward-only architecture - through self-renewal, loss of differentiation, or dedifferentiation - are more likely to acquire mutations and become malignant. Here, we use modeling to explore the consequences of differentiation architecture on evolution in cancer.

Published
2011

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