Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation

NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9...

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Published in:	Cancer discovery Vol. 12; no. 4; p. 1152
Main Authors:	Chandra, Bappaditya, Michmerhuizen, Nicole L, Shirnekhi, Hazheen K, Tripathi, Swarnendu, Pioso, Brittany J, Baggett, David W, Mitrea, Diana M, Iacobucci, Ilaria, White, Michael R, Chen, Jingjing, Park, Cheon-Gil, Wu, Huiyun, Pounds, Stanley, Medyukhina, Anna, Khairy, Khaled, Gao, Qingsong, Qu, Chunxu, Abdelhamed, Sherif, Gorman, Scott D, Bawa, Simranjot, Maslanka, Carolyn, Kinger, Swati, Dogra, Priyanka, Ferrolino, Mylene C, Di Giacomo, Danika, Mecucci, Cristina, Klco, Jeffery M, Mullighan, Charles G, Kriwacki, Richard W
Format:	Journal Article
Language:	English
Published:	United States 01.04.2022
Subjects:	Carcinogenesis Cell Nucleus Child Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Leukemia - genetics Nuclear Pore Complex Proteins - genetics Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Retinoblastoma-Binding Protein 2
ISSN:	2159-8290, 2159-8290
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Abstract	NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs. We show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873.
AbstractList	NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs.NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs.We show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873.SIGNIFICANCEWe show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873. NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs. We show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873.
Author	Pounds, Stanley Park, Cheon-Gil White, Michael R Michmerhuizen, Nicole L Qu, Chunxu Chen, Jingjing Mecucci, Cristina Dogra, Priyanka Iacobucci, Ilaria Khairy, Khaled Wu, Huiyun Baggett, David W Di Giacomo, Danika Klco, Jeffery M Maslanka, Carolyn Medyukhina, Anna Gao, Qingsong Abdelhamed, Sherif Kriwacki, Richard W Pioso, Brittany J Mitrea, Diana M Shirnekhi, Hazheen K Tripathi, Swarnendu Kinger, Swati Ferrolino, Mylene C Gorman, Scott D Chandra, Bappaditya Bawa, Simranjot Mullighan, Charles G
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Tennessee – sequence: 6 givenname: David W surname: Baggett fullname: Baggett, David W organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 7 givenname: Diana M surname: Mitrea fullname: Mitrea, Diana M organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 8 givenname: Ilaria orcidid: 0000-0003-2008-1365 surname: Iacobucci fullname: Iacobucci, Ilaria organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 9 givenname: Michael R surname: White fullname: White, Michael R organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 10 givenname: Jingjing orcidid: 0000-0003-4179-0371 surname: Chen fullname: Chen, Jingjing organization: Department of Hematology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 11 givenname: Cheon-Gil surname: Park fullname: Park, Cheon-Gil organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 12 givenname: Huiyun surname: Wu fullname: Wu, Huiyun organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 13 givenname: Stanley surname: Pounds fullname: Pounds, Stanley organization: Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 14 givenname: Anna orcidid: 0000-0001-5268-713X surname: Medyukhina fullname: Medyukhina, Anna organization: Center for Bioimage Informatics, St. Jude Children's Research Hospital Memphis, Tennessee – sequence: 15 givenname: Khaled orcidid: 0000-0002-9274-5928 surname: Khairy fullname: Khairy, Khaled organization: Center for Bioimage Informatics, St. Jude Children's Research Hospital Memphis, Tennessee – sequence: 16 givenname: Qingsong surname: Gao fullname: Gao, Qingsong organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 17 givenname: Chunxu surname: Qu fullname: Qu, Chunxu organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 18 givenname: Sherif orcidid: 0000-0002-3319-2403 surname: Abdelhamed fullname: Abdelhamed, Sherif organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 19 givenname: Scott D surname: Gorman fullname: Gorman, Scott D organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 20 givenname: Simranjot surname: Bawa fullname: Bawa, Simranjot organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 21 givenname: Carolyn surname: Maslanka fullname: Maslanka, Carolyn organization: Rhodes College, Memphis, Tennessee – sequence: 22 givenname: Swati orcidid: 0000-0002-2053-0944 surname: Kinger fullname: Kinger, Swati organization: Rhodes College, Memphis, Tennessee – sequence: 23 givenname: Priyanka surname: Dogra fullname: Dogra, Priyanka organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 24 givenname: Mylene C orcidid: 0000-0002-9693-8401 surname: Ferrolino fullname: Ferrolino, Mylene C organization: Department of Structural Biology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 25 givenname: Danika surname: Di Giacomo fullname: Di Giacomo, Danika organization: Department of Medicine and Surgery, University of Perugia, Perugia, Italy – sequence: 26 givenname: Cristina surname: Mecucci fullname: Mecucci, Cristina organization: Department of Medicine and Surgery, University of Perugia, Perugia, Italy – sequence: 27 givenname: Jeffery M orcidid: 0000-0003-2961-6960 surname: Klco fullname: Klco, Jeffery M organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 28 givenname: Charles G orcidid: 0000-0002-1871-1850 surname: Mullighan fullname: Mullighan, Charles G organization: Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee – sequence: 29 givenname: Richard W orcidid: 0000-0002-9798-6018 surname: Kriwacki fullname: Kriwacki, Richard W organization: Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Sciences Center, Memphis, Tennessee
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Snippet	NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered...
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SubjectTerms	Carcinogenesis Cell Nucleus Child Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Humans Leukemia - genetics Nuclear Pore Complex Proteins - genetics Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Retinoblastoma-Binding Protein 2
Title	Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation
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