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1. 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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2. 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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3. 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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4. 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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5. 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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6. 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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7. 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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9. 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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11. 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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12. In-Depth Characterization and Validation in BRG1-Mutant Lung Cancers Define Novel Catalytic Inhibitors of SWI/SNF Chromatin Remodeling

Author

Jagani, Zainab, primary, Chenail, Gregg, additional, Xiang, Kay, additional, Bushold, Geoffrey, additional, Bhang, Hyo-Eun C., additional, Li, Ailing, additional, Elliott, GiNell, additional, Zhu, Jiang, additional, Vattay, Anthony, additional, Gilbert, Tamara, additional, Bric, Anka, additional, Kikkawa, Rie, additional, Dubost, Valérie, additional, Terranova, Rémi, additional, Cantwell, John, additional, Luu, Catherine, additional, Silver, Serena, additional, Shirley, Matt, additional, Huet, Francois, additional, Maher, Rob, additional, Reece-Hoyes, John, additional, Ruddy, David, additional, Rakiec, Daniel, additional, Korn, Joshua, additional, Russ, Carsten, additional, Ruda, Vera, additional, Dooley, Julia, additional, Costa, Emily, additional, Park, Isabel, additional, Moebitz, Henrik, additional, Nakajima, Katsumasa, additional, Adair, Christopher D., additional, Mathieu, Simon, additional, Ntaganda, Rukundo, additional, Smith, Troy, additional, Farley, David, additional, King, Daniel, additional, Xie, Xiaoling, additional, Kulathila, Raviraj, additional, Hu, Tiancen, additional, Pan, Xuewen, additional, Ma, Qicheng, additional, Vulic, Katarina, additional, Rago, Florencia, additional, Clarkson, Scott, additional, Ge, Robin, additional, Sigoillot, Frederic, additional, Pardee, Gwynn, additional, Bagdasarian, Linda, additional, McLaughlin, Margaret, additional, Haas, Kristy, additional, Weiler, Jan, additional, Kovats, Steve, additional, Jaskelioff, Mariela, additional, Apolline-Gerard, Marie, additional, Beil, Johanna, additional, Naumann, Ulrike, additional, Fortin, Pascal, additional, Stegmeier, Frank P., additional, Acker, Michael G., additional, Williams, Juliet, additional, Meyer, Matthew, additional, Bradner, James E., additional, Keen, Nicholas, additional, Sellers, William R., additional, Hofmann, Francesco, additional, Engelman, Jeffrey A., additional, Stuart, Darrin, additional, and Papillon, Julien P.N., additional

Published
2019
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14. Distinct Organization and Regulation of the Outer Kinetochore KMN Network Downstream of CENP-C and CENP-T

Author

Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Cheeseman, Iain M, Rago, Florencia, Gascoigne, Karen E., Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Cheeseman, Iain M, Rago, Florencia, and Gascoigne, Karen E.

Abstract

The kinetochore provides a vital connection between chromosomes and spindle microtubules [1 and 2]. Defining the molecular architecture of the core kinetochore components is critical for understanding the mechanisms by which the kinetochore directs chromosome segregation. The KNL1/Mis12 complex/Ndc80 complex (KMN) network acts as the primary microtubule-binding interface at kinetochores [3] and provides a platform to recruit regulatory proteins [4]. Recent work found that the inner kinetochore components CENP-C and CENP-T act in parallel to recruit the KMN network to kinetochores [5, 6, 7 and 8]. However, due to the presence of these dual pathways, it has not been possible to distinguish differences in the nature of kinetochore assembly downstream of CENP-C or CENP-T. Here, we separated these pathways by targeting CENP-C and CENP-T independently to an ectopic chromosomal locus in human cells. Our work reveals that the organization of the KMN network components downstream of CENP-C and CENP-T is distinct. CENP-C recruits the Ndc80 complex through its interactions with KNL1 and the Mis12 complex. In contrast, CENP-T directly interacts with Ndc80, which in turn promotes KNL1/Mis12 complex recruitment through a separate region on CENP-T, resulting in functional relationships for KMN network localization that are inverted relative to the CENP-C pathway. We also find that distinct regulatory paradigms control the assembly of these pathways, with Aurora B kinase promoting KMN network recruitment to CENP-C and cyclin-dependent kinase (CDK) regulating KMN network recruitment to CENP-T. This work reveals unexpected complexity for the architecture and regulation of the core components of the kinetochore-microtubule interface., Leukemia & Lymphoma Society of America (Scholar Award), National Institutes of Health (U.S.) (National Institute of General Medical Sciences (U.S.). Grant GM088313), American Cancer Society (Research Scholar Grant 121776)

Published
2017

17. Organization and regulation of outer kinetochore assembly

Author

Iain M. Cheeseman., Massachusetts Institute of Technology. Department of Biology., Rago, Florencia, Iain M. Cheeseman., Massachusetts Institute of Technology. Department of Biology., and Rago, Florencia

Abstract

Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2015., This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections., Cataloged from student-submitted PDF version of thesis., Includes bibliographical references (pages 125-138)., The kinetochore provides the connection between chromosomes and spindle microtubules. Defining the molecular architecture of the core kinetochore components is critical for understanding the mechanisms by which the kinetochore directs chromosome segregation. The KNL1/Mis12 complex/Ndc80 complex (KMN) network acts as the primary microtubule-binding interface at kinetochores, and provides a platform for recruitment of regulatory proteins. The results in this thesis demonstrate that the CENP-C and CENP-T inner kinetochore receptors form separate scaffolds for KMN network assembly. Initial biochemical results suggested a non-canonical assembly pathway mediated by a direct interaction between CENP-T and the Ndc80 complex. These results were further verified and expanded upon in cells using an ectopic targeting approach to allow careful analysis of the pathways independently of one another. The data presented here demonstrate that in addition to forming two pathways, the CENP-C and CENP-T based assemblies are each constructed uniquely, showing both distinct organization of the KMN components as well as different modes of regulation. Analysis of the CENP-C based assembly pathway has previously defined the canonical architecture of the KMN network as a stable unit that associates with CENP-C via a direct interaction mediated by the Mis12 complex, and the data herein additionally shows that assembly of this pathway is regulated at least in part by Aurora B kinase activity. In contrast, the CENP-T protein forms a direct, CDK-dependent interaction with the Ndc80 complex, and this interaction is required for downstream recruitment of KNL1 and the Mis12 complex, resulting in a novel recruitment pathway for the KMN network. Together these results allow us to generate a new and more detailed molecular model for the assembly of the core structural components of the kinetochore., by Florencia Rago., Ph. D.

Published
2015

18. Kinetochore genes are coordinately up-regulated in human tumors as part of a FoxM1-related cell division program

Author

Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Kern, David Matthew, McKinley, Kara Lavidge, Monda, Julie Kathryn, Rago, Florencia, Cheeseman, Iain McPherson, Thiru, Prathapan, Su, Kuan-Chung, Tsinman, Tonia, Yarar, Defne, Bell, George W., Cheeseman, Iain M, Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Kern, David Matthew, McKinley, Kara Lavidge, Monda, Julie Kathryn, Rago, Florencia, Cheeseman, Iain McPherson, Thiru, Prathapan, Su, Kuan-Chung, Tsinman, Tonia, Yarar, Defne, Bell, George W., and Cheeseman, Iain M

Abstract

The key player in directing proper chromosome segregation is the macromolecular kinetochore complex, which mediates DNA–microtubule interactions. Previous studies testing individual kinetochore genes documented examples of their overexpression in tumors relative to normal tissue, leading to proposals that up-regulation of specific kinetochore genes may promote tumor progression. However, kinetochore components do not function in isolation, and previous studies did not comprehensively compare the expression behavior of kinetochore components. Here we analyze the expression behavior of the full range of human kinetochore components in diverse published expression compendia, including normal tissues and tumor samples. Our results demonstrate that kinetochore genes are rarely overexpressed individually. Instead, we find that core kinetochore genes are coordinately regulated with other cell division genes under virtually all conditions. This expression pattern is strongly correlated with the expression of the forkhead transcription factor FoxM1, which binds to the majority of cell division promoters. These observations suggest that kinetochore gene up-regulation in cancer reflects a general activation of the cell division program and that altered expression of individual kinetochore genes is unlikely to play a causal role in tumorigenesis., Leukemia & Lymphoma Society of America (Scholar Award), National Institute of General Medical Sciences (U.S.) (Grant GM088313), American Cancer Society (Research Scholar Grant 121776), National Science Foundation (U.S.). Graduate Research Fellowship

Published
2015

21. The functions and consequences of force at kinetochores

Author

Massachusetts Institute of Technology. Department of Biology, Massachusetts Institute of Technology. School of Science, Whitehead Institute for Biomedical Research, Rago, Florencia, Cheeseman, Iain McPherson, Cheeseman, Iain M, Massachusetts Institute of Technology. Department of Biology, Massachusetts Institute of Technology. School of Science, Whitehead Institute for Biomedical Research, Rago, Florencia, Cheeseman, Iain McPherson, and Cheeseman, Iain M

Abstract

Chromosome segregation requires the generation of force at the kinetochore—the multiprotein structure that facilitates attachment of chromosomes to spindle microtubules. This force is required both to move chromosomes and to signal the formation of proper bioriented attachments. To understand the role of force in these processes, it is critical to define how force is generated at kinetochores, the contributions of this force to chromosome movement, and how the kinetochore is structured and organized to withstand and respond to force. Classical studies and recent work provide a framework to dissect the mechanisms, functions, and consequences of force at kinetochores., National Institute of General Medical Sciences (U.S.) (Grant GM088313)

Published
2013

23. Kinetochore genes are coordinately up-regulated in human tumors as part of a FoxM1-related cell division program

Author

Iain M. Cheeseman, Julie K. Monda, David M Kern, Defne Yarar, Tonia Tsinman, Florencia Rago, Kuan-Chung Su, Prathapan Thiru, George W. Bell, Kara L. McKinley, Massachusetts Institute of Technology. Department of Biology, Whitehead Institute for Biomedical Research, Kern, David Matthew, McKinley, Kara Lavidge, Monda, Julie Kathryn, Rago, Florencia, and Cheeseman, Iain McPherson

Subjects
Cell division, Breast Neoplasms, Biology, medicine.disease_cause, Transcriptome, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, medicine, Humans, Kinetochores, Molecular Biology, Gene, 030304 developmental biology, Regulation of gene expression, Genetics, 0303 health sciences, Kinetochore, Carcinoma, Ductal, Breast, Forkhead Box Protein M1, Cell Cycle, Forkhead Transcription Factors, Cell Biology, Articles, Cell biology, Up-Regulation, Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, FOXM1, Female, Carcinogenesis, Cell Division
Abstract

The key player in directing proper chromosome segregation is the macromolecular kinetochore complex, which mediates DNA–microtubule interactions. Previous studies testing individual kinetochore genes documented examples of their overexpression in tumors relative to normal tissue, leading to proposals that up-regulation of specific kinetochore genes may promote tumor progression. However, kinetochore components do not function in isolation, and previous studies did not comprehensively compare the expression behavior of kinetochore components. Here we analyze the expression behavior of the full range of human kinetochore components in diverse published expression compendia, including normal tissues and tumor samples. Our results demonstrate that kinetochore genes are rarely overexpressed individually. Instead, we find that core kinetochore genes are coordinately regulated with other cell division genes under virtually all conditions. This expression pattern is strongly correlated with the expression of the forkhead transcription factor FoxM1, which binds to the majority of cell division promoters. These observations suggest that kinetochore gene up-regulation in cancer reflects a general activation of the cell division program and that altered expression of individual kinetochore genes is unlikely to play a causal role in tumorigenesis., Leukemia & Lymphoma Society of America (Scholar Award), National Institute of General Medical Sciences (U.S.) (Grant GM088313), American Cancer Society (Research Scholar Grant 121776), National Science Foundation (U.S.). Graduate Research Fellowship

Published
2014

24. The functions and consequences of force at kinetochores

Author

Iain M. Cheeseman, Florencia Rago, Massachusetts Institute of Technology. Department of Biology, Massachusetts Institute of Technology. School of Science, Whitehead Institute for Biomedical Research, Rago, Florencia, and Cheeseman, Iain McPherson

Subjects
Chromosome movement, 0303 health sciences, Kinetochore, Work (physics), Cell Biology, Biology, Spindle apparatus, Cell biology, Chromosome segregation, 03 medical and health sciences, 0302 clinical medicine, Microtubule, Mitosis, 030217 neurology & neurosurgery, 030304 developmental biology
Abstract

Chromosome segregation requires the generation of force at the kinetochore—the multiprotein structure that facilitates attachment of chromosomes to spindle microtubules. This force is required both to move chromosomes and to signal the formation of proper bioriented attachments. To understand the role of force in these processes, it is critical to define how force is generated at kinetochores, the contributions of this force to chromosome movement, and how the kinetochore is structured and organized to withstand and respond to force. Classical studies and recent work provide a framework to dissect the mechanisms, functions, and consequences of force at kinetochores., National Institute of General Medical Sciences (U.S.) (Grant GM088313)

Published
2012

25. Review series: The functions and consequences of force at kinetochores.

Author

Rago F and Cheeseman IM

Subjects
Animals, DNA metabolism, Humans, Kinetochores metabolism, Mitosis, Nuclear Proteins metabolism, Spindle Apparatus metabolism, Stress, Mechanical, Chromosome Segregation, Kinetochores physiology, Mechanotransduction, Cellular, Spindle Apparatus physiology
Abstract

Chromosome segregation requires the generation of force at the kinetochore-the multiprotein structure that facilitates attachment of chromosomes to spindle microtubules. This force is required both to move chromosomes and to signal the formation of proper bioriented attachments. To understand the role of force in these processes, it is critical to define how force is generated at kinetochores, the contributions of this force to chromosome movement, and how the kinetochore is structured and organized to withstand and respond to force. Classical studies and recent work provide a framework to dissect the mechanisms, functions, and consequences of force at kinetochores.

Published
2013
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